The American Journal of Cardiology

Published by Elsevier
Borderline increase of troponin I (cTnI) is associated with higher rates of cardiovascular events compared with normal levels in the setting of acute coronary syndrome (ACS), but the significance of borderline cTnI levels in patients without chest pain may differ. The aim of this study was to determine the prognostic implications of intermediate serum cTnI levels in patients without ACS in the intensive care unit (ICU). This was a 12-month retrospective study of 240 patients without ACS in the ICU with normal (<0.1 ng/ml) or intermediate (0.1 to 1.49 ng/ml) cTnI levels. End points included in-hospital mortality, lengths of ICU and hospital stays, and rates of postdischarge readmission and mortality. Overall in-hospital mortality was 13%, with 5% in the normal cTnI group and 28% in the intermediate cTnI group. By multivariate analysis, intermediate cTnI was independently associated with in-hospital mortality (p = 0.004) and length of ICU stay (p = 0.028). The only other independent risk factor for inpatient mortality was a standardized ICU prognostic measurement (Simplified Acute Physiology Score II score). Intermediate cTnI had no prognostic implications regarding length of hospital stay, readmission rate, or postdischarge mortality at 6 months. In conclusion, an intermediate level of cTnI in patients without ACS in the ICU is an independent prognostic marker predicting in-hospital mortality and length of ICU stay. Patients with intermediate cTnI levels who survive to discharge have equivalent out-of-hospital courses for up to 6 months compared with patients with normal cTnI levels.
One hundred eighty-seven patients with clinically documented supraventricular tachycardia with a narrow QRS complex were admitted for electrophysiologic study. The diagnoses after this study were circus movement tachycardia using an accessory pathway in 50 patients, atrioventricular nodal tachycardia in 50 patients, atrial flutter in 50 patients, atrial tachycardia in 27 patients and an incessant tachycardia retrogradely using a slowly conducting accessory pathway in 10 patients. On retrospective analysis, 5 criteria on the 12-lead electrocardiogram during tachycardia were analyzed for their value in making the diagnosis of site of origin. These criteria were P-wave location, axis of the P wave, atrial rate, alternation of the QRS complex and atrioventricular relation. Fifty-seven patients with a narrow QRS tachycardia were prospectively studied using the 5 criteria. A correct diagnosis was made in 48 of the 57 patients (84%). Thus, in most patients with a narrow QRS tachycardia, information from the 12-lead electrocardiogram is adequate for diagnosis.
In patients with stable coronary artery disease, elevated levels of biomarkers of inflammation, including high-sensitivity C-reactive protein (hs-CRP) > or = 2.0 mg/L, are predictors of future vascular events. Because long-term low-dose colchicine is a safe and effective means of dampening inflammation, we conducted an open-label pilot study to determine whether it could significantly lower hs-CRP in patients with stable coronary artery disease in whom hs-CRP was > or = 2.0 mg/L despite taking both aspirin and high-dose atorvastatin therapy. Plasma hs-CRP was measured in 200 patients with clinically stable coronary artery disease who were taking aspirin and atorvastatin. In 64 patients, hs-CRP was > or = 2.0 mg/L. In 20 of these patients, hs-CRP was measured again at 2 weeks (no treatment group), and in 44 patients, hs-CRP was measured again after 4 weeks of open-label colchicine 0.5 mg twice daily (treatment group). In the no treatment group, mean baseline hs-CRP did not decrease significantly, measuring 4.28 +/- 2.03 mg/L at baseline and 3.70 +/- 2.30 mg/L after repeated measurement (mean change 11.0%, 95% confidence interval [CI] -30% to +9%, p = NS). In contrast, hs-CRP decreased in all patients administered colchicine, with mean baseline hs-CRP decreasing from 4.58 +/- 2.05 to 1.78 +/- 1.38 mg/L (p <0.001), an absolute decrease of 2.80 mg/L (95% CI 2.40 to 3.65 mg/L) and a relative decrease of 60% (95% CI 54% to 67%). In 28 patients (64%) in this group, the decrease in hs-CRP was >50% from baseline, and in 31 patients (70%), hs-CRP decreased to <2.0 mg/L. No significant side effects were reported. In conclusion, low-dose colchicine (0.5 mg twice daily) can effectively decrease hs-CRP in patients with clinically stable coronary artery disease and increased hs-CRP independent of aspirin and atorvastatin use. Additional controlled studies are warranted to confirm this observation and determine whether long-term use of low-dose colchicine can improve clinical outcomes in patients with advanced vascular disease.
We prospectively evaluated all patients admitted to our coronary care unit during 1993 with ischemic chest pain but without ST-segment elevation on the presenting electrocardiogram, and determined the influence of the extent of ST-segment depression, measured using calipers and blinded to the outcome, on 4-year survival. The presenting symptoms of 367 patients (mean age 64 years) were coded according to the Braunwald classification, 86% being in class IIIB (primary unstable angina with rest angina within 48 hours) and 7.4% in class IIIC (postinfarction angina). Thirty-two patients (8.6%) had myocardial infarction at presentation (defined as a creatine kinase level exceeding twice the reference range within 18 hours). During hospitalization 97% of patients received aspirin, 67% received intravenous heparin, 37% underwent angiography, and 35% underwent revascularization. The vital status of 99% of the patients was determined after a median of 52 months (interquartile range 48 to 55). At follow-up, 88% of patients were taking aspirin, 45% were taking beta blockers, and 50% had undergone revascularization. The survival rate was 70% in patients with > or = 0.5-mm ST-segment depression (53%, 77%, and 82% survival for > or = 2-, 1-, and 0.5-mm ST-segment depression, respectively; p <0.0001). Patients with a normal electrocardiogram had a greater survival rate (94%) than that of patients with 0.5-mm ST-segment depression (82%, p = 0.020), but not significantly different from that of patients with T-wave inversion (84%, p = NS). Independent predictors of mortality (odds ratio [95% confidence interval]) were: age in yearly increments (1.05 [1.03 to 1.06], p = 0.003), revascularization during follow-up (0.40 [0.29 to 0.56], p = 0.006), pulmonary edema (3.45 [2.19 to 5.45], p = 0.007), and ST-segment depression (1.37 [1.20 to 1.55], p = 0.015). Thus, ST-segment depression of > or = 0.5 mm predicts 4-year survival in patients with acute ischemic syndromes.
To determine whether arteriographic dimensions of the acutely recanalized coronary lumen provide information about regional perfusion or clinical outcome, quantitative arteriography was used to measure minimum luminal diameter achieved with intracoronary streptokinase administration in 44 patients with acute myocardial infarction (AMI). Degree of coronary reperfusion was independently assessed visually using the criteria applied in the multicenter Thrombolysis in Myocardial Infarction study. Minimum diameter and qualitative reperfusion grade were both assessed from 172 coronary injections during thrombolysis. Partial perfusion (grade 1 or 2) was seen in 95 of 135 injections (70%) in which the minimum diameter was less than 0.6 mm and complete perfusion (grade 3) was seen in 35 of 37 injections (95%) in which it was 0.6 mm or more (p less than 0.001). Repeat cardiac catheterization was performed at 5.5 +/- 4.9 weeks after AMI (n = 20). When vessels were opened acutely to a minimum diameter of less than 0.6 mm, 5 of 12 vessels (42%) were reoccluded at the time of restudy and 8 of 29 patients (28%) died within 12 months. By contrast, 0 of 8 vessels (0%) were reoccluded when the artery was opened to a diameter of at least 0.6 mm (difference not significant), and only 1 of 15 patients (7%) died (p less than 0.05). Of the patients with grade 1 o r 2 perfusion at the end of the thrombolytic infusion, 7 of 19 (37%) died within 12 months and 2 of 4 vessels (50%) reoccluded; of the patients with grade 3 perfusion, 2 of 25 (8%) died (p less than 0.05) and 2 of 16 vessels (13%) reoccluded (difference not significant).(ABSTRACT TRUNCATED AT 250 WORDS)
Eighty-four patients with suspected coronary artery disease were studied to determine the accuracy of noninvasive coronary angiography using a multidetector computed tomographic scanner with 64- x 0.6-mm collimation and 330-ms gantry rotation. All coronary artery segments with a diameter >1.5 mm were assessed with respect to stenoses >50% decreased diameter. Results were compared with quantitative coronary angiographic findings. After exclusion of unevaluable coronary segments (4%), multidetector computed tomography demonstrated a sensitivity of 93%, a specificity of 97%, and a negative predictive value of 100% in a per-segment analysis. In a per-artery analysis, 15 of 336 arteries (4%) were unevaluable. Sensitivity and specificity in evaluable arteries were 95% and 93%, respectively. In a per-patient analysis (81 of 84 patients included), sensitivity and specificity were 96% and 91%, respectively.
Cerivastatin is a third generation hydroxy-methyl-glutaryl-Co-enzyme A (HMG-CoA) reductase inhibitor proven to lower low-density lipoprotein (LDL) cholesterol 28% to 31% in patients with primary hypercholesterolemia when given at 0.3 mg/day. This study evaluates the safety, tolerability, pharmacodynamics, and pharmacokinetics of cerivastatin 0.8 mg once daily for 4 weeks. In this randomized, double-blind, placebo-controlled parallel group trial conducted at 2 study centers, 41 patients (63% women) with primary hypercholesterolemia were placed on an American Heart Association Step 1 diet for 4 weeks. Single-blind placebo was administered for the final 2 weeks, before randomization. Patients received cerivastatin 0.8 mg (n = 28) or placebo (n = 13) once each evening for 28 days. Cerivastatin at 0.8 mg daily was well tolerated. No discontinuations occurred during the study. Adverse events were mild and transient. One cerivastatin-treated patient experienced asymptomatic creatinine kinase, 8x the upper limit of normal (ULN) elevation on the last day of the study, which resolved 6 days after the completion of the study. Cerivastatin 0.8 mg daily significantly reduced LDL cholesterol compared with placebo (-44.0 +/- 2.0% vs 2.2 +/- 2.8%, p <0.0001); total cholesterol (-30.8 +/- 1.4% vs 2.6 +/- 2.1%, p <0.0001), triglycerides (-11.2 +/- 5.9% vs 15.9 +/- 8.6%, p <0.02), but did not significantly alter high-density lipoprotein (HDL) cholesterol (3.2 +/- 2.1% vs -1.2 +/- 3.1%, p = NS). The pharmacokinetics of the 0.8-mg dose revealed dose proportional elevations in the 24-hour area under the curve and maximum plasma concentration relative to 0.3- and 0.4-mg doses with no change in time to maximum concentration or the elimination half-life in plasma. The increased efficacy and lack of clinically significant laboratory abnormalities or adverse events demonstrates a need for a large long-term study to confirm the safety and efficacy of this dose of cerivastatin.
"Trough" plasma concentrations of isosorbide-5-mononitrate (IS-5-MN), an active metabolite of isosorbide dinitrate, of less than 95 ng/ml are considered necessary to prevent development of tolerance to isosorbide dinitrate and IS-5-MN. In a double-blind, crossover, placebo-controlled study, the effects of IS-5-MN during twice daily eccentric therapy were evaluated in 18 patients with reproducible exercise-induced angina who were nitrate responders. In a random order, patients received either placebo or IS-5-MN (20 mg) at 8 a.m. and 2 p.m. for 1 week each. Average trough plasma IS-5-MN concentrations before the 8 a.m. and 2 p.m. doses were 67 and 226 ng/ml, respectively, and increased to 382 and 488 ng/ml 2 hours after the 8 a.m. and 2 p.m. doses, respectively. Despite a more than threefold higher trough plasma IS-5-MN concentration before the 2 p.m. dose than before the 8 a.m. dose, the increase in exercise duration 2 hours after the doses was similar (1.21 minutes [21%] after 8 a.m. dose, and 1.08 minutes [19%] after 2 p.m. dose). These increases in exercise duration after IS-5-MN were significantly (p less than 0.01) greater than those observed after placebo (0.17 minutes [3%] after 8 a.m. dose, and -0.05 minute [-0.5%] after 2 p.m. dose). Reduction in standing systolic blood pressure at 2 hours after the doses was also nearly identical after the 8 a.m. and 2 p.m. doses of IS-5-MN (21 [15%] and 19 [14%] mm Hg, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
This retrospective analysis reviewed 183 patients with acute myocardial infarction who were given front-loaded recombinant tissue-type plasminogen activator (rt-PA) and r-hirudin (HBW 023) in 1 of 4 dose groups (bolus dose of 0.07, 0.1, 0.2, or 0.4 mg/kg, followed by an infusion of 0.05, 0.06, 0.1, or 0.15 mg/kg/hour over 48 hours). Activated partial thromboplastin time (aPTT) levels were determined at baseline and at 4, 8, 12, 16, 20, 24, 32, 40, and 48 hours. Of the 178 patients with r-hirudin treatment for > or = 12 hours, anticoagulation was optimal in 55.1% (all aPTTs > 2 x baseline), suboptimal in 33.7% (lowest aPTT > 1.5 but < 2 x baseline), and inadequate in 11.2% (> or = 1 aPTT but < 1.5 x baseline). Optimal anticoagulation was observed more frequently in the higher dose groups (dose 1, 15%; dose 2, 44.4%; dose 3, 63.4%; dose 4, 73.4%; p for trend < 0.0001). Patency (according to Thrombolysis in Myocardial Infarction trial grade 2 or 3) of the infarct artery after 36 to 48 hours was higher in the group with optimal anticoagulation compared with those with suboptimal or inadequate anticoagulation: 97.9%, 88.4%, and 85%, respectively (p = 0.03 optimal vs suboptimal or inadequate anticoagulation). In conclusion, r-hirudin in a dose of 0.1 or 0.15 mg/kg/hour achieves an optimal anticoagulation in about 63% or 74% of patients, which is associated with an enhanced patency 24 to 48 hours after rt-PA. A subsequent study revealed that this effective anticoagulation may be accompanied by an increased risk of severe bleeding complications after thrombolysis.
The novel recombinant plasminogen activator (r-PA) (BM 06.022) is a mutant of tissue-type plasminogen activator expressed in escherichia coli which can be given as a bolus because of a prolonged half-life. The primary objective of this trial was to determine the efficacy of an intravenous r-PA double bolus (first bolus of 10 MU followed by 5 MU after 30 minutes) in patients with acute myocardial infarction. All patients received heparin intravenously and acetylsalicylic acid orally. Efficacy was assessed from infarct artery patency by coronary angiography (Thrombolysis in Myocardial Infarction trial perfusion grades 2 or 3) in 50 patients. Ninety minutes after administration of the first r-PA bolus, the infarct-related coronary artery was patent in 39 of 50 patients (78%; 95% confidence interval 64 to 88%). An angiographically confirmed reocclusion occurred in 1 patient between 90 minutes and 24 to 48 hours. The reocclusion rate was influenced by 8 interventions and 1 angiogram missing at 24 to 48 hours. Measurements of hemostatic parameters showed a decrease in fibrinogen to 37% of baseline value. There were 3 clinical reinfarctions before discharge and 2 major puncture site hemorrhages. No further serious bleeding and no serious adverse event with lethal outcome occurred. The 10 + 5 MU r-PA double bolus regimen appears to be effective with regard to patency and the success of thrombolysis. The incidence of reocclusion is very low. From the limited number of patients treated in this study, one need not be concerned about the safety profile of r-PA.
A new inotropic agent, TA-064, (-)-α-(3,4-dimethoxyphenethylaminomethyl)-4-hydroxybenzylalcohol, was shown to have strong effects in experimental animals. Its effectiveness and associated adverse effects were tested in humans invasively (n = 6) and noninvasively (n = 17). Increasing doses of intravenous infusion (1, 2, and 4 μg/kg/min) increased plasma levels to 15, 35, and 82 ng/ml, respectively, resulting in marked increases in the peak rate of left ventricular pressure rise (dP/dt) (1,450 ± 63 to 3,042 ± 349 mm Hg/s) (mean ± standard error of the mean [SEM], p <0.01) and the ratio of dP/dt to left ventricular pressure at a developed pressure of 40 mm Hg (25 ± 3 to 39 ± 2 s-1) (p <0.01), with a reduction in left ventricular end-diastolic pressure (12 ± 2 to 4 ± 1 mm Hg) (p <0.01). Minimal or no changes were seen in heart rate and left ventricular systolic pressure. After a single oral dose (10 mg), the plasma level reached its peak at 90 minutes (16 ± 9 ng/ml, n = 17). A positive inotropic effect was confirmed echocardiographically in both healthy volunteers (n = 8) and patients with congestive heart failure (CHF) (n = 9) who were maximally treated with conventional regimens: increase in mean velocity of circumferential fiber shortening (healthy volunteers: 1.29 ± 0.05 to 1.60 ± 0.11 circ/s [p < 0.05]; patients with CHF: 0.69 ± 0.08 to 0.93 ± 0.09 circ/s [p <0.01]), ejection fraction (healthy volunteers: 68 ± 2 to 75 ± 2% [p <0.05], patients with CHF: 37 ± 4 to 45 ± 5% [p <0.01]) without change in heart rate. The cardiac index was increased only in the CHF group (2.71 ± 0.22 to 3.21 ± 0.24 liters/min/m2) (p <0.05). No significant untoward effects were observed. Thus TA-064 is a potent inotropic agent and can be used either parenterally or orally. Salutary effects can be expected in patients with congestive heart failure who are treated with digitalis and diuretic agents.
Stent thrombosis and restenosis remain drawbacks of drug-eluting stents in patients with acute myocardial infarction (AMI). Intravascular ultrasound (IVUS) guidance for stent deployment helps optimize its results in stable patients. The aim of this study was to examine the utility of routine IVUS guidance in patients with AMI undergoing percutaneous coronary intervention (PCI). Employing data from Korea Acute Myocardial Infarction Registry (KAMIR), we analyzed 14,329 patients with AMI from April 2006 through September 2010. Patients with cardiogenic shock and rescue PCI after thrombolysis were excluded. Clinical outcomes of 2,127 patients who underwent IVUS-guided PCI were compared to those of 8,235 patients who did not. Mean age was 63.6 ± 13.5 years and 72.3% were men. Patients undergoing IVUS-guided PCI were younger, more often men, more hyperlipemic, and had increased body mass index and left ventricular ejection fraction. Number of treated vessels and stents used, stent length, and stent diameter were increased in the IVUS-guided group. Multivessel involvement was less frequent and American College of Cardiology/American Heart Association type C lesion was more frequent in the IVUS-guided group. Drug-eluting stents were more frequently used compared to bare-metal stents in the IVUS group. There was no significant relation of stent thrombosis between the 2 groups. Twelve-month all-cause death was lower in the IVUS group. After multivariate analysis and propensity score adjustment, IVUS guidance was not an independent predictor for 12-month all-cause death (hazard ratio 0.212, 0.026 to 1.73, p = 0.148). In conclusion, this study does not support routine use of IVUS guidance for stent deployment in patients who present with AMI and undergo PCI.
The efficacy of PY 108-068 (75 and 150 mg/day), a new dihydropyridine calcium antagonist, was compared with placebo for treatment of chronic stable angina. Twelve patients were studied in a placebo-controlled, double-blind, randomized, crossover trial of 2 weeks each. Antianginal efficacy was assessed by the number of episodes of angina and nitroglycerin tablets consumed during each 2-week period, as well as the number of episodes of ischemia during 48-hour ambulatory monitoring and the area and severity of ST-segment depression during 16-point precordial exercise mapping. Nitroglycerin consumption (mean +/- standard error of the mean) decreased from 6.1 +/- 2.9 with placebo to 1.8 +/- 1.5 with 75 mg/day of PY 108-068 (p less than or equal to 0.03) and to 3.6 +/- 2.3 with 150 mg/day of PY 108-068 (p less than or equal to 0.01 vs placebo, difference not significant vs 75 mg/day of PY 108-068), whereas episodes of angina were reduced significantly only by the high dose (p less than or equal to 0.03) (11.1 +/- 3.9 with placebo, 6.3 +/- 2.4 with 75 mg/day of PY 108-068 and 8.1 +/- 3.4 with 150 mg/day of PY 108-068). The low dose alone significantly reduced ST-segment depression during exercise testing (p less than or equal to 0.03) (29.6 +/- 3.6 with placebo, 23.1 +/- 5.6 with 75 mg/day of PY 108-068 and 24.4 +/- 5.0 with 150 mg/day of PY 108-068), whereas neither dose significantly altered the number of episodes of ischemia during ambulatory monitoring.(ABSTRACT TRUNCATED AT 250 WORDS)
The current status of 997 of 1,000 consecutive children with a cardiac malformation initially evaluated between 1952 and 1963 was determined. Of the 1000, 285 have died and the survivors have been followed up for periods of 26 to 37 years. Six hundred thirty-two are in excellent or good clinical condition, being asymptomatic and without planned need for further treatment. The other 80 have significant abnormalities, although 63 of these have few symptoms. Infective endocarditis occurred in 12 of 10,000 susceptible patient-years, with a lower rate in the past decade. Only 22 of the survivors are currently receiving cardiac medication. These data are derived from a group of patients initially seen during a period of time that cardiac surgery was being developed for congenital heart disease. Thus, the outlook should be even better for children who are currently undergoing treatment.
In a consecutive series of 1,000 women under age 50 examined by coronary cinearteriography principally for evaluation of chest pain, 236 had at least 50 percent narrowing of one or more coronary arteries. The youngest, and the only patient who died, was 26 years old. The anterior descending coronary artery was the vessel most frequently involved; the right coronary artery was most often totally occluded. The amount of arterial involvement seemed to be related to the duration of symptoms. Only 10 percent of women with serum cholesterol levels under 200 mg/100 ml had significant coronary artery disease, whereas 44 percent of those with levels over 275 mg/100 ml had significant disease. Electrocardiographic evidence of myocardial infarction was uncommon in women with single vessel disease, but left ventriculograms disclosed that additional patients had areas of decreased contractility. Eleven of 46 women with electrocardiographically diagnosed myocardial infarction had no significant coronary artery disease. The cause of the electrocardiographic finding remained obscure in some. Although there was an excellent correlation of clinical diagnoses with arteriographic findings in women thought not to have angina pectoris, only half of those thought to have angina pectoris had significant coronary artery disease. This finding may be a major reason for recommending coronary arteriography for the evaluation of angina-like pain in women under age 50.
From 1952 to 1963, 1,000 consecutive children with congenital heart disease were evaluated by 1 of us (R.C.A.). Current information for 994 patients with 36,086 patient-years is available. Of these, 362 have died, 130 as adults, of whom 67 died from a cardiac cause. Of the remaining 638 patients, 632 were living, and 6 were lost to follow-up. The survival curves for ventricular septal defect, atrial septal defect, patent ductus arteriosus, and pulmonary stenosis paralleled the normal curve. Cyanotic patients had a markedly reduced curve, with 19% alive at 50 years. Most patients were New York Heart Association class I, with only 3 in class IV, each from noncardiac causes. In conclusion, this experience should be helpful to physicians caring for adults with congenital heart disease and provide an optimistic outlook for the patients with less complex conditions.
Certain clinical and morphologic features are described in 23 patients in whom the heart at necropsy weighed at least 1,000 g (mean 1,106). The heart weight to body weight ratio ranged from 1.2 to 2.7 (normal 0.40). The 23 patients were derived from examination of the hearts of 7,671 patients with various cardiovascular disorders over a 25-year period. The massive cardiomegaly was the result of aortic regurgitation in 14 patients (61%): isolated in 8, associated with mitral regurgitation in 4, and with ventricular septal defect in 2. Three others (13%) had combined aortic valve stenosis and aortic regurgitation and 1 patient (4%) had mitral stenosis and regurgitation and mild aortic stenosis. Four patients (17%) had hypertrophic cardiomyopathy, and 1 patient (4%) had ventricular septal defect with mitral stenosis. They were 20 to 64 years old (mean 42) and 21 (91%) were men. Four patients at necropsy had 1 or more major coronary arteries narrowed more than 75% in cross-sectional area by atherosclerotic plaques, and only 4 patients had grossly visible left ventricular (LV) scars, 2 of whom had insignificant coronary narrowing. Examination of electrocardiograms in 17 of the 23 patients disclosed that Sokolow-Lyon criteria for LV hypertrophy was achieved in only 12 patients (71%) and Romhilt-Holt QRS voltage criteria faired even worse. Total 12-lead QRS voltage was more than 175 mm (10 mm = 1 mV) in 16 patients (94%) and it was more than 250 mm in 13 patients (76%). Total 12-lead QRS voltage in 17 patients ranged from 140 to 601 mm (mean 323). Measurement of the sum of the 12-lead QRS voltage may be quite useful in diagnosing LV hypertrophy by electrocardiogram.
Abciximab decreases adverse cardiac ischemic events, and in some subgroups, decreases the need for revascularization after percutaneous coronary intervention (PCI). However, abciximab may cause bleeding complications and thrombocytopenia after PCI. We hypothesized that the efficacy and safety of PCI would be maintained, if not improved, when performed using abciximab accompanied by only minimal doses (< or =1,000 U) of unfractionated heparin. In this prospectively designed observational study, we assessed 500 consecutive patients who underwent PCI, consisting of either stent deployment or high-speed rotational atherectomy, and who received abciximab accompanied by only a minimal dose of unfractionated heparin, as directed by a novel dosing strategy: (1) if the patient was previously receiving an infusion of heparin, then it was terminated upon arrival to the cardiac catheterization laboratory, and no further heparin was administered; or (2) if the patient was not receiving an infusion of heparin, then a single bolus infusion of 1,000 U was administered after establishment of vascular access. The median activated clotting time for the patients during PCI was 168 seconds (25% quartiles, 153 to 185). The technical success rate was 99.8%. There were no major adverse clinical events during the 24 hours after PCI. The incidence of non-Q-wave myocardial infarction was 1.6%. The incidences of major and minor bleeding complications were 0.2% and 3.6%, respectively, and the incidence of thrombocytopenia was 2.2%. During the 30 days after PCI, there was 1 major adverse clinical event (0.2%). During the 1 year after PCI, among the remaining patients, there were 92 adverse events (18.4%). We conclude that, in the context of historical data, the efficacy and safety of PCI using either stent deployment or high-speed rotational atherectomy is maintained, if not improved, when performed using abciximab accompanied by only minimal doses of unfractionated heparin.
Primary angioplasty (direct angioplasty without antecedent thrombolytic therapy) has remained an exclusive and consistent method of infarct intervention at our institution over the past 13 years. A total of 1,000 consecutive patients were prospectively enrolled in our primary angioplasty database. Of patients presenting to our group with an acute myocardial infarction, 96% of those eligible received immediate angioplasty. Cardiogenic shock was noted in 79 patients (7.9%). The mean time from pain onset to reperfusion was 5.4 +/- 4.0 hours. Infarct-vessel recanalization was accomplished in 94% of patients. Recanalization rates were similar among the 3 native epicardial coronary systems but were lower in bypass grafts (86%; p < 0.0001). Overall in-hospital mortality was 7.8%; mortality with cardiogenic shock was 44%. Global ejection fraction increased from 49.7% preangioplasty to 57.4% at the time of dismissal. The amount of myocardial salvage was highly dependent on the size of the initial infarction (the largest infarctions benefiting the most). Patients reperfused in < 2 hours experienced a very low mortality (4%) and impressive myocardial salvage. Complications included stroke in 0.5%, significant bleeding in 2.8%, and early reocclusion of the infarct vessel in 13%. Primary angioplasty is broadly applicable to patients presenting with acute myocardial infarction and results in a very high rate of infarct vessel recanalization, with a mortality rate of 7.8%. This strategy may be uniquely effective in patients presenting with cardiogenic shock, large infarctions, contraindications to thrombolytic therapy, and prior bypass surgery.
We evaluated the efficacy and safety of elective percutaneous coronary intervention (PCI) at a hospital without onsite cardiac surgery. A growing number of hospitals without onsite cardiac surgery perform elective PCI. Few hospitals have reported outcomes, despite controversy surrounding this practice. From August 2003 to December 2005, 1,090 elective PCI were performed at Saint Luke's South Hospital (SLS), a hospital without onsite cardiac surgery, for which the referral center is the Mid America Heart Institute (MAHI). The elective PCI program used experienced interventionalists, technicians, and nurses; a tested helicopter transport protocol; a well-equipped catheterization laboratory; and a quality assurance process. Baseline characteristics, procedural success, and adverse clinical outcomes were compared. Observed frequencies of in-hospital death, a combined end point of Q-wave myocardial infarction (MI)/emergency coronary artery bypass grafting (CABG) surgery, and vascular complications were compared with prediction models. SLS, with lower risk characteristics than MAHI, had unadjusted frequencies of procedural success (93% vs 94%, p = NS), Q-wave MI (0.3% vs 0.3%, p = NS), emergency CABG surgery (0.2% vs 0.03%, p = 0.09), vascular complications (0.6% vs 0.6%, p = NS), and in-hospital death (0.1% vs 0.8%, p = 0.002) that compared favorably with MAHI. Two patients transferred from SLS to MAHI for emergency CABG surgery without adverse effects. Fewer in-hospital deaths and vascular complications were observed at SLS than predicted by models. In conclusion, favorable clinical outcomes were achieved for elective PCI at a hospital without onsite cardiac surgery that used strict program requirements.
Ischemic ST-segment depression on the resting electrocardiogram has been related to increased cardiovascular mortality.1–5 This prospective study correlated ischemic ST-segment depression on the resting electrocardiogram with development of new cardiac events in unselected patients older than 62 years.
One thousand one hundred twenty-three percutaneous mitral valvotomy procedures performed in 1,086 patients between 1989 and 2000 were analyzed prospectively, comparing different age groups. Although hemodynamic and functional improvement was greater in younger patients, the intervention appeared to be a safe and effective procedure also in older patients, many of whom had moderate or significant valvular calcification.
To determine the influence of coronary bypass surgery on late survival, 1,144 consecutive patients were contacted 60 to 76 months after operation. There were 1,000 men (87.4 percent). The mean age was 50.1 years (range 24 to 75). Operation was performed for angina pectoris with coronary lesions of more than 70 percent reduction in luminal diameter in 1,101 patients (96.2 percent). Forty-three patients (3.8 percent) had congestive heart failure without angina and 240 (21.0 percent) had both heart failure and angina. Unstable angina was present in 149 patients (13 percent). Previous myocardial infarction had occurred in 675 patients (59 percent). Single vessel disease was present in 226 patients (19.8 percent), double vessel disease in 442 (38.6 percent), triple vessel disease in 376 patients (32.9 percent) and greater than 50 percent stenosis of the left main coronary artery in 100 patients (8.7 percent). The overall operative mortality rate was 4.6 percent (52 patients). With exclusion of patients with left main coronary artery disease, this rate was 3.8 percent (40 of 1,044) and the overall crude 5 year survival rate was 89.1 percent (930 of 1,044). The survival rates of men and women were comparable. Left ventricular function was classified as good if end-diastolic pressure was less than 15 mm Hg and the left ventriculogram revealed no aneurysmal or akinetic area. Among men, the respective survival rates for each subgroup and for those with good left ventricular function within that subgroup were as follows: one vessel disease, 92.9 percent (169 of 182) and 94.9 percent (130 of 137); two vessel disease, 90.3 percent (352 of 390) and 94.3 percent (248 of 263); three vessel disease, 85.7 percent (293 of 342) and 90.9 percent (189 of 208); left main coronary artery disease, 81.4 percent (70 of 86) and 90.6 percent (48 of 53). The graft patency rate in 157 patients was 86.4 percent (247 of 286 grafts), and 149 patients (94.9 percent) had at least one patent graft.
The prevalence of mitral regurgitation, valvular aortic stenosis, aortic regurgitation, hypertrophic cardiomyopathy, idiopathic dilated cardiomyopathy, and of left ventricular hypertrophy was not significantly different in older men and women. Older women had a significantly higher prevalence of rheumatic mitral stenosis, mitral annular calcium, and left atrial enlargement than older men, and older men had a significantly higher prevalence of abnormal left ventricular ejection fraction than older women.
A prospective study performed in 1,311 men and women, mean age 81 years, with heart disease and sinus rhythm showed at 48-month follow-up that male sex, increasing age, and average 24-hour heart rate measured from 24-hour ambulatory electrocardiograms were independent risk factors for new coronary events. There was a 1.14 times higher chance of developing new coronary events for an increment of 5 beats/min of heart rate after controlling the confounding effect of other risk factors.
Early studies of a cobalt-based alloy stent coated with the novel antiproliferative agent zotarolimus and a phosphorylcholine polymer have demonstrated significant reductions in angiographic restenosis and target vessel revascularization compared with bare metal stents. However, the generalizability of the angiographic outcomes and clinical benefit of zotarolimus-eluting stents (ZESs) to a more real-world patient population is undetermined. Clinical and angiographic outcomes in 1,317 patients treated with the ZES in the first 4 trials of the Endeavor ZES (Medtronic Vascular, Santa Rosa, CA) clinical trials program were pooled for systematic analysis. Protocol-specified follow-up angiography was performed at 8 or 12 months for a subset of 750 of these patients, and clinical follow-up was performed at 9 months after the index procedures in all patients. Diabetes mellitus was present in 22.5% of patients, the mean reference vessel diameter was 2.73 mm, and the mean lesion length was 14.59 mm. At 8 months (12 months for ENDEAVOR I), mean +/- SD in-stent late luminal loss was 0.61 +/- 0.49 mm. In-stent late luminal loss was greatest in larger caliber (>2.9 mm) vessels (0.65 +/- 0.49 mm) and longer (>16.3 mm) lesions (0.70 +/- 0.52 mm) but did not statistically vary according to diabetic status. At 9 months, overall rates of target lesion revascularization (TLR) and major adverse cardiac events (MACE) were 4.9% and 7.7%, respectively. The rate of TLR at 12 months was not significantly different relative to diabetes and lesion length >16.3 mm (7.2% and 7.7%, respectively), although TLR was significantly more common when reference vessel diameter was <2.5 mm (8.5%; p = 0.013). At 24 months, overall rates of TLR and MACE were 6.5% and 9.9%, respectively. The overall 24-month rate of stent thrombosis was 0.3%, with no events occurring >14 days after the procedure. Despite varied clinical and angiographic characteristics, treatment with the ZES is associated with consistently low rates of TLR and overall major adverse events, including stent thrombosis. Although these findings indicate the efficacy and safety of the ZES over the time course of the first 4 ENDEAVOR clinical trials, additional ongoing study with more open patient inclusion criteria (including long lesions, small vessels, bifurcations, etc) will be important for discerning whether comparable clinical outcomes can be extended to lesion subsets of higher complexity.
Despite controversy, a growing body of data exists suggesting that percutaneous coronary intervention (PCI) with no surgical onsite availability is safe and efficacious. Over a period of 3 years all patients requiring PCI had their intervention performed at the Launceston General Hospital, a regional hospital serving rural Tasmania, Australia. There were no exclusion criteria uniformly adopted. Primary end points included angiographic success and major procedure-related complications. A total cohort of 1,348 consecutive patients underwent PCI during the calendar years of 2005 through 2007, including patients with ST-elevation myocardial infarction. Angiographic success for all patients was >98%. In-hospital mortality was 0.8% overall. Only 1 patient required urgent transfer to a cardiac surgical center. Bleeding rates requiring transfusion were approximately 1%. Excellent clinical outcomes have been achieved in a relatively remote PCI center in rural, northern Tasmania, where there is no emergency cardiac surgical availability. Angiographic success was high and complication rates were low, consistent with worldwide standards. In conclusion, PCI without onsite surgery appears safe and efficacious when well-trained staffing is available.
The Framingham Study reported that the incidence of deaths from cardiovascular causes was 43% in men with atrial fibrillation and 21% in men with sinus rhythm (risk ratio = 2.0), and 41% in women with atrial fibrillation and 15% in women with sinus rhythm (risk ratio = 2.7).1 At 34-month mean follow-up of 118 patients with global T-wave inversion, Walder and Spodick6 demonstrated that the mortality rate was 58% in 12 patients with atrial fibrillation detected by electrocardiograms, and 35% in 106 patients with sinus rhythm (p = 0.005). Data from this study show that atrial fibrillation is an independent predictor of new coronary events in elderly patients with heart disease. The time to onset of new coronary events was also significantly shorter in patients with atrial fibrillation than in patients with sinus rhythm or supraventricular tachycardia. After controlling for other prognostic variables, patients with atrial fibrillation and heart disease had a 2.2 times higher probability of developing new coronary events than those with heart disease without atrial fibrillation.
Amlodipine is a light-insensitive and water soluble 1,4-dihydropyridine with prolonged vasodilatory action and plasma half-life. To determine whether the vasodilatory action of amlodipine is due to inhibition of voltage-dependent Ca2+ influx through the calcium channel, its effects on KCl-induced contraction of pig coronary artery rings and its interaction with the 1,4-dihydropyridine binding site in isolated sarcolemmal membranes were studied. The contractile function of artery rings was studied in an organ bath system, and the interaction with the 1,4-dihydropyridine binding site was studied in isolated sarcolemmal membranes of pig coronary artery using [3H](+)PN200-110 as a radioligand. Amlodipine, (+)PN200-110 and (-)PN200-110 inhibited KCl-induced contractions of arterial rings in a dose-dependent manner. The half-maximal inhibition (IC50) was observed at 0.46 +/- 0.02, 36 +/- 8 and 55 +/- 9 nM of (+)PN200-110, (-)PN200-110 and amlodipine, respectively. [3H](+)PN200-110 was found to bind to isolated sarcolemmal membranes with high affinity (KD = 0.04 nM, Bmax = 312 fmoles/mg protein) and stereospecifically, (+)PN200-110 (Ki = 0.05 nM) having about 130-fold higher affinity than (-)PN200-110 (Ki = 6.61 nM). Amlodipine also inhibited [3H](+)PN200-110 binding with high affinity (Ki = 4.41 nM). The inhibition was characterized by an increase in KD of binding of [3H](+)PN200-110 with very little effect on Bmax. The order of relative potency of inhibition of KCl-induced contraction was almost identical to the order of relative affinity for the 1,4-dihydropyridine binding site, as indicated by Ki.(ABSTRACT TRUNCATED AT 250 WORDS)
The effects of a new 1,4-dihydropyridine derivative amlodipine have been compared with results from our previous work. Application of amlodipine at a concentration of 1.6 X 10(-6) M to isolated guinea-pig papillary muscle for 120 minutes produced a 50% reduction in tension development compared with a concentration of 3.7 X 10(-7) M nifedipine needed to produce the same result under identical conditions. This suggests that amlodipine has even weaker negative inotropic effects than nifedipine. In isolated porcine coronary strips, the K+-induced contractions were approximately 10,000 times more sensitive to the relaxing effects of nisoldipine, nitrendipine and nicardipine than to those of papaverine, whereas nifedipine and amlodipine were 3,000 times more potent than papaverine. However, in comparison with these in vitro actions, the efficacy of amlodipine appears to be greater in vivo: Simultaneous subcutaneous injection of nifedipine (20 mg/kg) and of equimolar doses of nisoldipine and felodipine attenuated the myocardial calcium uptake by rat hearts in situ (stimulated with a single subcutaneous dose of 30 mg/kg isoproterenol) with the same efficacy, whereas the actions of nitrendipine and nimodipine were considerably weaker. In contrast, amlodipine antagonized isoproterenol-stimulated myocardial calcium accumulation more effectively. Furthermore, amlodipine exhibited a high antihypertensive potency combined with rapid onset and long duration of action: Amlodipine (10 mg/kg orally [p.o.]) reduced the blood pressure of spontaneously hypertensive rats almost to the same extent as nifedipine, nitrendipine, verapamil and felodipine administered at the much higher doses of 100 mg/kg p.o. Amlodipine (20 mg/kg/day p.o.) maintained normal blood pressure during the whole life span of Dahl-S rats (5 months), but this dose is considerably lower than that reported for other 1,4-dihydropyridines. The survival of NaCl-loaded Dahl-S rats increased from 20 to 100% after administration of amlodipine (20 mg/kg/day p.o.) over 10 weeks: The effective dose of other calcium antagonists is approximately 5 times higher, but well tolerated as, e.g., demonstrated in long-term studies on Dahl-S rats with nitrendipine over 12 months. Increases in systemic arteriolar tone can be visualized in the ocular fundus of spontaneously hypertensive rats. After amlodipine (10 mg/kg p.o.) arteriolar spasm declines. Prophylaxis with 2 doses of 20 mg/kg amlodipine daily in NaCl-loaded Dahl-S rats abolished the macroscopic and histologic changes that are normally seen in branches of the mesenteric artery. With use of electron microscopy, calcium accumulation in the lamina elastica interna was demonstrated by the potassium-pyr-oantimonate technique.(ABSTRACT TRUNCATED AT 400 WORDS)
Patients with documented coronary artery disease, admitted to Duke Medical Center between 1974 and 1980, were assessed for type A behavior pattern and were followed until 1984. The relation of type A behavior to survival was tested using data from coronary angiography to control for disease severity. Cox model regression analyses demonstrated an interaction (p less than 0.01) between type A behavior and an index of disease severity in the prediction of cardiovascular death. Among those with relatively poor left ventricular function, type A patients had better survival than type B. This difference was not present among patients with better prognoses. Type A behavior did not predict the subsequent incidence of nonfatal myocardial infarctions. Differential risk modification and differential selection into postinfarction status are possible explanations for the findings. These results need not conflict with the proposition that type A behavior plays a role in the pathogenesis of coronary artery disease.
Comparison of 239 older patients with 40% to 100% extracranial carotid arterial disease (ECAD) with 1,243 older patients with no significant ECAD showed a higher prevalence of systemic hypertension, left ventricular (LV) hypertrophy, and prior atherothrombotic brain infarction (ABI) and a higher incidence of new ABI in patients with ECAD than in patients without ECAD. A multivariate Cox regression model showed that independent predictors of new ABI were ECAD (risk ratio = 2.5), systemic hypertension (risk ratio = 2.3), prior ABI (risk ratio = 2.3), LV hypertrophy (risk ratio = 2.3), and male sex (risk ratio = 1.3).
The relation between obesity and new ABI is also unclear. The Framingham Study found that relative weight was not a risk factor for new ABI in older men but was a weak risk factor for new ABI in older women. Barrett-Connor and Khaw found no association between body mass index and new ABI in older men or women. The present study showed that obesity was not a risk factor for new ABI in older men. Obesity was a risk factor for new ABI in older women by univariate analysis but not by multivariate analysis. However, because obesity is associated with other risk factors for ABI and new coronary events, we would try to lower weight in obese older men and women.
Acute hemodynamic and electrocardiographic effects of fructose-1,6-diphosphate (FDP), an agent that is supposed to restore anaerobic glycolytic flux in the ischemic myocardium, were studied in 40 patients with acute myocardial infarction who were grouped into 4 subsets: subset 1, normal (15 mm Hg or less) pulmonary artery (PA) wedge pressure and normal (35 g-m/m2 or greater) left ventricular (LV) stroke work index; subset 2, elevated (more than 15 mm Hg) PA wedge pressure and normal LV stroke work index; subset 3, normal PA wedge pressure and reduced (less than 35 g-m/m2) LV stroke work index; subset 4, elevated PA wedge pressure and LV stroke work index moderately reduced to a range between 16 and 34 g-m/m2. Patients were randomized into an FDP (250 mg/kg body weight in isotonic saline solution intravenously in 20 minutes) and into a placebo group. Each subset contained 5 FDP- and 5 placebo-treated patients. After basal measurements, hemodynamic measurements were reassessed at 60, 90 and 120 minutes from the infusions, while a standard 12-lead electrocardiogram was recorded in the basal state and 120 minutes after infusion. Nonsignificant hemodynamic change was observed in the placebo subsets, and FDP failed to exert any effect in subsets 1, 2 and 3. A 24% (p less than 0.02) increase in cardiac index occurred 60 minutes after FDP in subset 4. LV stroke work index also increased, while PA wedge pressure remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
In the present study, elderly patients with chronic atrial fibrillation had a 2.9 times higher prevalence of left atrial enlargement, a 2.0 times higher prevalence of LV hypertrophy, and a 2.5 times higher prevalence of abnormal LV ejection fraction than elderly patients with sinus rhythm.
Revised Appropriate Use Criteria (AUC) for Echocardiography were published in 2011 and classify potential procedure indications as appropriate (score of 7 to 9), uncertain (score of 4 to 6), or inappropriate (score of 1 to 3). The appropriate utilization rate of transthoracic echocardiography in clinical practice using the revised AUC is unknown. The aim of the present study was to determine the appropriate utilization rate of echocardiography in a large number of consecutive studies in clinical practice and to determine the number of "unclassifiable" studies using the revised and expanded AUC. The clinical indication for transthoracic echocardiography (TTE) was determined on the basis of a detailed review of preprocedural clinical documentation. These clinical indications were further classified (when possible) into 1 of the 98 indications described in the 2011 AUC for echocardiography. From December 2010 to January 2011, 1,825 patients (mean age 63.2 years) underwent TTE for clinical reasons. Of the final study group of 1,820 patients, TTE was appropriate in 82%, inappropriate in 12.3%, and uncertain in 5.3%, and 0.4% studies were unclassifiable. The evaluation of symptoms potentially due to a cardiac etiology was the most common appropriate indication for TTE (27.5%). The most common inappropriate indication was routine surveillance (<1 year) of heart failure without a change in clinical status (2.5%). In conclusion, most TTE studies were appropriately ordered, and only a very small number of studies were unclassifiable.
In a prospective study of 1,846 persons, mean age 81 +/- 8 years, 281 persons (15%) had 40% to 100% extracranial carotid arterial disease and 253 persons (14%) had chronic atrial fibrillation. The Cox regression model showed that significant independent risk factors for new thromboembolic stroke were atrial fibrillation (p = 0.0001, risk ratio 3.3), 40% to 100% extracranial carotid arterial disease (p = 0.0001, risk ratio 2.5), prior stroke (p = 0.0001, risk ratio 2.1), and male gender (p = 0.045, risk ratio 1.2).
In an initial retrospective study, covering 3 years, 30 (3 percent) of 966 patients consecutively discharged from the coronary care unit, were found to have sustained late in-hospital ventricular fibrillation 10 to 38 days after myocardial infarction. Of these 30 patients, 18 (60 percent) died in the hospital and 14 (47 percent) had anteroseptal infarction complicated by right or left bundle branch block. In a later prospective study, covering 2 1 2 years, 47 consecutive coronary care unit survivors with anteroseptal infarction complicated by right or left bundle branch block were kept in the monitoring area for 6 weeks after infarction. Seventeen of these 47 (36 percent) sustained late in-hospital ventricular fibrillation. Neither the type nor the duration of bundle branch block affected the Incidence of late in-hospital ventricular fibrillation. Six (35 percent) of the 17 patients with ventricular fibrillation died in the hospital. Three died from ventricular fibrillation, and of six patients treated with infarctectomy, another three died postoperatively. Of 11 hospital survivors with late in-hospital ventricular fibrillation, followed up for 1 to 30 months, 1 died suddenly within 1 month. Of the remaining 884 patients who were not kept in the monitoring area after coronary care unit discharge, 8 (0.9 percent) sustained late ventricular fibrillation (with 3 in-hospital deaths) and 4 (0.5 percent) others died suddenly in hospital. The results indicate that coronary care unit survivors with anteroseptal infarction complicated by right or left bundle branch block should be kept in the monitoring area for 6 weeks.
Our study indicates that the combination of nicotinic acid (1.2 g/day) and lovastatin (20 mg/day) is more effective than either drug alone in reducing total and LDL cholesterol. Although HDL cholesterol was not significantly improved by these doses of agents over the duration of this study, LDL/HDL and HDL/total cholesterol ratios were improved due to the beneficial actions on total and LDL cholesterol. No serious side effects or changes in serum chemistries were observed, and the combination was well tolerated.
Conventional pacemaker and implantable cardioverter-defibrillator product labeling currently cautions against exposure to magnetic resonance imaging (MRI). However, there is a growing clinical need for MRI, without an acceptable alternative imaging modality in many patients with cardiac devices. The purpose of this study was to determine the risk of MRI at 1.5 T for patients with cardiac devices by measuring the frequency of device failures and clinically relevant device parameter changes. Data from a single-center retrospective review of 109 patients with pacemakers and implantable cardioverter-defibrillators (the MRI group) who underwent 125 clinically indicated MRI studies were compared to data from a prospective cohort of 50 patients with cardiac devices who did not undergo MRI (the control group). In the MRI group, there were no deaths, device failures requiring generator or lead replacement, induced arrhythmias, losses of capture, or electrical reset episodes. Decreases in battery voltage of ≥0.04 V occurred in 4%, pacing threshold increases of ≥0.5 V in 3%, and pacing lead impedance changes of ≥50 Ω in 6%. Although there were statistically significant differences between the MRI and control groups for the mean change in pacing lead impedance (-6.2 ± 23.9 vs 3.0 ± 22.1 Ω) and left ventricular pacing threshold (-0.1 ± 0.3 vs 0.1 ± 0.2 V), these differences were not clinically important. In conclusion, MRI in patients with cardiac devices resulted in no device or lead failures. A small number of clinically relevant changes in device parameter measurements were noted. However, these changes were similar to those in a control group of patients who did not undergo MRI.
The relation between glomerular filtration rate (GFR) <60 ml/min/1.73 m(2) and the extent and progression of coronary atherosclerosis in 989 subjects with coronary artery disease was investigated. Despite being older, more likely to be women, and having a history of hypertension, diabetes, and bypass surgery, total atheroma volume and percent atheroma volume in subjects with a low GFR did not differ from subjects with a GFR >60 ml/kg/min. Similarly, there was no difference in progression rates of total atheroma volume and percent atheroma volume in patients with GFRs lower and higher than 60 ml/min/1.73 m(2) in response to a high rate of use of established preventive therapies. In conclusion, findings suggest that the increased incidence of clinical events in patients with impaired renal function may result from factors other than atherosclerotic burden.
Clinical cardiovascular evaluations were performed on 508 school children living at 10,150 feet in Leadville, Colo. The electrocardiograms of 493 of these children were analyzed and the findings were compared with electrocardiographic observations on similar residents at various altitudes. Thirty per cent of the subjects had electrocardiographic findings suggestive of right ventricular enlargement. The average mean ÂQRS of the entire group was more rightward that that of children of similar age living at 5,280 feet and at sea level, and less rightward than that of teenage children living at 14,900 feet. Electrocardiographic variability is an important part of the clinical evaluation of the healthy teenage subject living at high altitude.
A circadian variation of symptom onset in acute myocardial infarction (AMI) with an increased frequency in the late morning and possibly also in the evening has been found in several studies. It has been suggested that different circadian rhythms may exist in various subgroups of patients. This possibility was examined in a population of 10,791 patients collected between 1973 and 1987 in a continuously operating register of patients with AMI in Malmö, Sweden. In 6,763 patients (63%) in whom a distinct symptom onset could be established, symptom onset occurred with an increased frequency between 6:01 A.M. and 12:00 noon (30.6%) and between 6:01 P.M. and 12:00 midnight (26.9%). Similar bimodal circadian rhythms were seen in patients aged greater than 70 years (n = 2,923), less than or equal to 70 years (n = 3,840), men (n = 4,528), women (n = 2,235), smokers (n = 2,458), hypertensives (n = 1,999), diabetics (n = 653), patients with (n = 1,872) and without (n = 4,891) a history of previous AMI, and in patients with recent non-Q-wave AMI (n = 333). In 455 patients receiving cardioselective beta blockers the circadian distribution did not differ from a random, whereas in patients taking nonselective beta blockers or calcium antagonists significant bimodal rhythms were found. Statistically significant interactions were found between symptom onset and age dichotomized at 70 years, and between patients with and without a history of previous AMI. In a multivariate analysis only these variables age less than or equal to/greater than 70 years; +/- history of a previous AMI) were found to modify the circadian rhythm of symptom onset in the population.(ABSTRACT TRUNCATED AT 250 WORDS)
Top-cited authors
William Clifford Roberts
  • Baylor Health Care System
Daniel Levy
  • National Heart, Lung, and Blood Institute
Wilbert S Aronow
  • New York Medical College
Mark E Josephson
  • Brigham and Women's Hospital
Patrick W Serruys
  • National University of Ireland, Galway / Imperial College London