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ABSTRACT: Sudden cardiac death and myocardial infarction have a circadian variation with a peak incidence in the early morning hours. Increased dispersion of repolarization facilitates the development of conduction delay necessary to induce sustained arrhythmia. Both QT-dispersion and T-wave peak to T-wave end (TpTe) have been proposed as markers of dispersion of myocardial repolarization.
Forty healthy adults (20 women), age 35-67 years old, with normal EKGs, echocardiograms, stress tests, and tilt-table tests were analyzed during a 27-hour hospital stay. EKGs were done at eight different time points. QT-intervals, QT-dispersion, and TpTe were measured at each time point. Harmonic regression was used to model circadian periodicity, P < 0.05 was considered significant.
The composite QT-interval was longer in women than in men (416 + or - 17 msec vs 411 + or - 20 msec, respectively, P = 0.006). The QT-dispersion among all leads was greater in men than women (37 + or - 13 msec vs 30 + or - 11 msec, respectively, P < 0.0001); a similar difference was found in the precordial leads. Harmonic regression showed that QT-dispersion had a significant circadian variation, primarily in men. In men, the maximum QT-dispersion occurred at 6 AM (45 + or - 15 msec). TpTe also had a significant circadian variation that was not affected by gender in the majority of leads.
A circadian variation exists in the dispersion of myocardial repolarization, as measured by both TpTe and QT-dispersion. Men and women have a different circadian variation pattern. Further studies regarding the mechanisms and clinical implications are needed.
Annals of Noninvasive Electrocardiology 01/2010; 15(1):3-10. · 1.10 Impact Factor
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ABSTRACT: The goal in treating carotid artery atherosclerotic disease is to reduce the risk of stroke. Three therapeutic options for
management of carotid disease exist: medical therapy, carotid artery stenting, and carotid endarterectomy. Clinical and anatomic
characteristics of the individual patient dictate which of these options should be chosen. This chapter will review the indications
and contraindications to carotid artery stenting.
KeywordsIndications–Contraindications–Reimbursement–Training requirement–Credentialing
12/2008: pages 111-120;
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ABSTRACT: Left main (LM) coronary disease, carotid artery disease, and peripheral arterial disease each reflects advanced atherosclerosis. The frequency of their coexistence in the same patient has not been fully elucidated. All coronary angiograms obtained at the Cleveland Clinic from November 2003 to October 2005 were analyzed for presence of LM stenosis > or =50%. Patients with previous coronary artery bypass graft surgery were excluded. Patients with available carotid ultrasound and ankle-brachial indexes formed the analysis cohorts. A total of 10,298 coronary angiograms were obtained in 9,715 patients. There were 186 patients with LM disease and 1,913 patients without LM disease with carotid artery ultrasound data. There were 29 patients with LM disease and 604 patients without LM disease with available ankle-brachial indexes. Patients with significant LM disease more frequently had associated carotid stenosis > or =60% compared with patients without LM disease (31.2% vs 15.2%, p <0.0001). Patients with LM disease had lower mean ankle-brachial indexes compared with patients without LM disease (0.78 vs 0.87, p = 0.042). In conclusion, compared with patients without LM disease, patients with LM disease have a higher burden of advanced atherosclerosis as evidenced by a higher prevalence of significant carotid stenosis and lower ankle-brachial indexes.
The American Journal of Cardiology 11/2007; 100(7):1087-9. · 3.37 Impact Factor
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Annals of internal medicine 03/2007; 146(3):230-2. · 16.73 Impact Factor
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ABSTRACT: We examined the safety and efficacy of nonculprit multivessel compared with culprit-only stenting in patients with multivessel disease presenting with unstable angina or non-ST-segment elevation myocardial infarction (non-ST-segment elevation acute coronary syndromes [NSTE-ACS]).
In patients presenting with NSTE-ACS, multivessel coronary artery disease (CAD) is associated with adverse outcome.
Patients with multivessel CAD and NSTE-ACS that underwent percutaneous coronary intervention were included. The culprit lesion was defined by reviewing each patient's angiographic report, electrocardiogram, echocardiogram and, if available, nuclear stress test. All patients had at least 2 vessels with > or =50% stenosis, and the angiographic severity of CAD was assessed using the Duke Prognostic Angiographic Score. Patients with coronary bypass grafts, chronic total occlusions, and those with uncertain culprit lesions were excluded. Our end point was the composite of death, myocardial infarction, or any target vessel revascularization.
From January 1995 to June 2005, 1,240 patients with ACS and multivessel CAD underwent percutaneous coronary intervention with bare-metal stenting and met our study criteria. Of these, 479 underwent multivessel and 761 underwent culprit-only stenting. There were 442 events during a median follow-up of 2.3 years. Multivessel intervention was associated with lower death, myocardial infarction, or revascularization after both adjusting for baseline and angiographic characteristics (hazard ratio 0.80; 95% confidence interval 0.64 to 0.99; p = 0.04) and propensity matched analysis (hazard ratio 0.67; 95% confidence interval 0.51 to 0.88; p = 0.004).
In patients with multivessel CAD presenting with NSTE-ACS, multivessel intervention was significantly associated with a lower revascularization rate, which translated to a lower incidence of the composite end point compared with culprit-only stenting.
Journal of the American College of Cardiology 03/2007; 49(8):849-54. · 14.16 Impact Factor
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ABSTRACT: Platelet glycoprotein (GP) IIb/IIIa inhibitors are widely used in percutaneous coronary intervention (PCI). Previous studies have suggested that they do not offer benefit in saphenous vein graft PCI. Nonetheless, their use remains widespread during vein graft angioplasty. We retrospectively analyzed 1,537 patients who underwent saphenous vein graft PCI. Patients who received a GP IIb/IIIa inhibitor (n = 941) were compared with those who did not receive any GP IIb/IIIa inhibitor (n = 596). The primary end point was myonecrosis after PCI (creatine kinase-MB level >3 times the upper reference limit). The incidence of myonecrosis after PCI was similar between the group that received GP IIb/IIIa and the group that did not (odds ratio for GP IIb/IIIa use 1.39, 95% confidence interval 0.97 to 2.00, p = 0.07). Propensity-adjusted analysis demonstrated no significant difference in myonecrosis after PCI, in-hospital mortality, Q-wave myocardial infarction, or bleeding (blood transfusion, retroperitoneal bleed, or hematoma) between the 2 groups. In an analysis restricted to patients who were treated with an emboli protection device, GP IIb/IIIa use was not associated with decreased myonecrosis after PCI (this was also the case for patients who were not treated with an emboli protection device). Unadjusted survival (mean follow-up 5.5 +/- 0.1 years) was similar between the group that received GP IIb/IIIa and the group that did not (log-rank test, p = 0.89). There was no difference in survival after adjusting for the propensity to receive a GP IIb/IIIa inhibitor (adjusted odds ratio for GP IIb/IIIa use 0.92, 95% confidence interval 0.69 to 1.23, p = 0.59). In conclusion, adjunctive use of platelet GP IIb/IIIa inhibitors in saphenous vein graft PCI does not appear to be associated with less myonecrosis or improved survival.
The American Journal of Cardiology 11/2006; 98(7):906-10. · 3.37 Impact Factor
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ABSTRACT: Previous observations in the bare metal stent (BMS) era have demonstrated an association between a high preprocedural C-reactive protein (CRP) level and an increased incidence of death or myocardial infarction after percutaneous coronary intervention (PCI). We hypothesized that PCI with sirolimus-eluting stents (SESs) would result in a smaller increase in CRP compared with BMSs and that a high CRP level before PCI would be associated with a higher incidence of death or myocardial infarction at 12 months, regardless of the type of stent implanted. We analyzed patients who underwent PCI with stenting at the Cleveland Clinic Foundation. Patients who received BMSs and SESs were analyzed separately by categorizing them into low and high CRP groups based on whether their CRP level before PCI was above or below the median for each group. The increase in CRP that occurred with PCI was termed DeltaCRP. In total, 652 patients were included in the analysis. Median DeltaCRP was smaller in the SES group than in the BMS group (1.5 vs 0.7 mg/L, p = 0.009). In the BMS group, patients with a CRP level above the median before PCI had a higher incidence of 12-month death or myocardial infarction compared with patients with a CRP level below the median (11.3% vs 1.6%, p = 0.002). The same relation was present in the SES group, i.e., patients with a higher CRP level had a higher incidence of 12-month death or myocardial infarction compared with patients with a low CRP level (6.3% vs 1.0%, p = 0.005) and a higher 12-month mortality (5.2% vs 0%, p = 0.001). Multivariate logistic regression analysis demonstrated that the CRP level above the median before PCI was associated with a higher 12-month incidence of death or myocardial infarction, independent of the type of stent used, or DeltaCRP. In conclusion, PCI in the SES era causes a smaller increase in CRP compared with the BMS era. A high CRP level before PCI is independently associated with a higher risk of long-term death or myocardial infarction. This finding was present in the BMS and SES groups and highlights the need for aggressive risk-factor modification after PCI.
The American Journal of Cardiology 10/2006; 98(5):616-8. · 3.37 Impact Factor
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ABSTRACT: Aspirin inhibits platelet aggregation and is widely used in the treatment of cardiovascular disease. Some individuals are less responsive to aspirin's antiplatelet effect, a phenomenon termed aspirin resistance. It is not known whether the antiplatelet effect is fully preserved with the enteric-coated (EC) formulation.
We performed a prospective randomized trial of 50 healthy volunteers using a crossover design to compare the EC with the standard aspirin formulations. The subjects received a 7-day course of each aspirin formulation (81-mg) (Bayer Corporation, Morristown, NJ) separated by a 3-week washout period. Platelet function was measured before and after each course using optical aggregometry (with arachidonic acid and adenosine diphosphate as agonists) and a point-of-care platelet assay.
The assays were reproducible, and the variation in baseline platelet function was small to moderate between the subjects. There was no difference in the extent of platelet inhibition between the EC and standard formulations with any of the 3 assays. With the point-of-care platelet assay, the mean aspirin effect favoring the standard formulation (more aggregation inhibition) compared with the EC formulation was 1.6% +/- 15.8% (P = .60 for difference between the formulations). The corresponding optical aggregometry values were -3.4% +/- 39.5% (P = .97) and -1.4% +/- 16.6% (P = .75) for arachidonic acid and adenosine diphosphate, respectively.
Compared with standard aspirin, EC aspirin appears to exhibit similar inhibition of platelet aggregation in healthy volunteers. Furthermore, point-of-care platelet assessment correlated well with the gold standard of laboratory-based optical platelet aggregometry.
American heart journal 06/2006; 151(5):976.e7-11. · 4.65 Impact Factor
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ABSTRACT: Patients with acute myocardial infarction (MI) with ST-segment elevation have better outcomes with primary percutaneous coronary intervention (PCI) than with fibrinolytic therapy. Multiple clinical trials in the past 10 years have addressed ways to improve PCI as primary therapy for acute MI. Logistic strategies to improve access to PCI are being studied.
Cleveland Clinic Journal of Medicine 08/2005; 72(7):559-60, 562, 565-6 passim. · 3.77 Impact Factor
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ABSTRACT: In patients who undergo primary percutaneous coronary intervention (PCI), poor post-PCI myocardial blush is associated with increased mortality, even when epicardial perfusion is adequate. This observation has important implications for the methods of evaluating primary PCI results and the strategies used to improve myocardial reperfusion.
The American Journal of Cardiology 05/2005; 95(8):980-2. · 3.37 Impact Factor
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American heart journal 04/2005; 149(3):384-7. · 4.65 Impact Factor
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ABSTRACT: Patients (n = 1,106) were chosen from the conservative arm of the Treat Angina with aggrastat and determine Cost of Therapy with an Invasive or Conservative Strategy-Thrombolysis In Myocardial Infarction (TACTICS-TIMI) 18 trial. Only 1 patient had a myocardial infarction and another died on the day of stress testing (mortality 0.12%). In patients with unstable angina pectoris or non-ST-elevation myocardial infarction treated with aspirin, heparin, and tirofiban, performance of an exercise or a pharmacologic stress test in selected patients within 48 to 72 hours after admission appears to be associated with a low risk of complications.
The American Journal of Cardiology 01/2005; 94(12):1537-9. · 3.37 Impact Factor
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Cleveland Clinic Journal of Medicine 01/2005; 71(12):933-4, 936, 938-9. · 3.77 Impact Factor
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Reviews in Endocrine and Metabolic Disorders 09/2004; 5(3):277-85. · 3.17 Impact Factor
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C Michael Gibson, Juhana Karha,
Robert P Giugliano,
Mathew T Roe,
Sabina A Murphy,
Robert A Harrington,
Cindy L Green,
Marc J Schweiger,
Jerry S Miklin,
Kenneth W Baran,
Sebastian Palmeri,
Eugene Braunwald,
Mitchell W Krucoff
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ABSTRACT: More complete ST-segment resolution (ST res) in acute myocardial infarction (MI) has been associated with better epicardial and myocardial reperfusion as assessed with the Thrombolysis in Myocardial Infarction (TIMI) flow grade (TFG) and the TIMI myocardial perfusion grade (TMPG), respectively. However, no data exist comparing the speed of ST resolution on continuous electrocardiogram (ECG) monitoring with the TMPG on coronary angiography. We hypothesized that delayed ST res is associated with impaired TMPGs.
Continuous 12-lead ECG recordings and 60-minute angiographic data were analyzed in 120 patients with acute MI who received tenectaplase monotherapy or combination therapy with low-dose tenectaplase and eptifibatide in the Integrilin and Tenecteplase in Acute Myocardial Infarction (INTEGRITI) trial.
More rapid ST res on continuous ECG monitoring was associated with improved TMPGs on coronary angiography performed 60 minutes after study drug administration. For TMPG 3, the median time to ST resolution was 53 minutes. For TMPG 2, 1, and 0, the corresponding times were 64 minutes, 80 minutes, and 106 minutes, respectively (P =.01 for trend). Likewise, more rapid ST res was also associated with faster epicardial flow. For TFG 3, the median time to ST resolution was 46 minutes, compared with 109 minutes for TIMI flow grades 0 to 2 (P =.001). The corresponding times for a corrected TIMI frame count < or =40 versus >40 were 52 minutes and 112 minutes, respectively (P <.001).
Although the static ECG has been associated with epicardial and myocardial blood flow in the past, this study extends these observations to demonstrate that more rapid ST res on continuous ECG monitoring is associated with improved myocardial perfusion after thrombolytic administration.
American heart journal 06/2004; 147(5):847-52. · 4.65 Impact Factor
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C Michael Gibson, Juhana Karha,
Sabina A Murphy,
James A de Lemos,
David A Morrow,
Robert P Giugliano,
Mathew T Roe,
Robert A Harrington,
Christopher P Cannon,
Elliott M Antman,
Robert M Califf,
Eugene Braunwald
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ABSTRACT: We hypothesized that recognition of systolic flow reversal (pulsatile flow) after thrombolytic administration on coronary angiography is associated with angiographic and electrocardiogram findings reflecting impaired myocardial perfusion, as well as poorer clinical outcomes.
Reversal of systolic flow on Doppler velocity wire recordings has been associated with impaired tissue perfusion on myocardial contrast echocardiography in the setting of myocardial infarction (MI).
Patients (n = 1,062) with a patent infarct-related artery were drawn from the Thrombolysis In Myocardial Infarction (TIMI) 10, TIMI 14, and Integrillin and Tenecteplase acute MI trials.
Pulsatile flow (systolic flow reversal with cessation of antegrade contrast-dye motion or frank reversal of contrast-dye motion during systole) at 60 min after fibrinolytic administration was present in 11.0% of patients. Pulsatile flow was associated with higher corrected TIMI frame counts (slower epicardial flow) (median 40.1 frames, IQ 30 of 63 vs. 30 frames, interquartile 22 of 42, p < 0.0001), a closed microvasculature (TIMI myocardial perfusion grades 0 of 1, 57.1% vs. 37.8%, p = 0.03) and less complete (> or =70%) ST-segment resolution (23.5% vs. 58.9%, p = 0.008). Patients with pulsatile flow had a higher risk of death or reinfarction at 30 days (10.3% vs. 5.0%, p = 0.019). After controlling for age, pulse, blood pressure, anterior MI location, epicardial flow, and creatine kinase, pulsatile flow remained associated with an increased risk of death/MI (odds ratio 3.1, p = 0.006).
A pulsatile pattern of flow is associated with impaired myocardial perfusion and poorer clinical outcomes independent of the velocity of antegrade flow in the epicardial artery. This simple and easily identifiable angiographic flow pattern may be useful in clinical risk stratification.
Journal of the American College of Cardiology 04/2004; 43(7):1170-6. · 14.16 Impact Factor
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C Michael Gibson,
William J Gibson,
Sabina A Murphy,
Susan J Marble,
Carolyn H McCabe,
Minang P Turakhia,
Ajay J Kirtane, Juhana Karha,
Julian M Aroesty,
Robert P Giugliano,
Elliott M Antman
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ABSTRACT: This is the first study to demonstrate the appearance of the Fibonacci Cascade within the distribution of coronary artery lesions in the human heart. The propensity for this ratio to appear in nature may also be because this ratio optimizes the efficiency of packing structures in a limited space in such a way that wasted space is minimized and the supply of energy or nutrients is optimized.
The American Journal of Cardiology 10/2003; 92(5):595-7. · 3.37 Impact Factor
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ABSTRACT: Impaired coronary artery blood flow and left anterior descending (LAD) artery culprit location are angiographic variables that have been associated with poorer outcomes after fibrinolytic administration in patients with acute myocardial infarction (AMI). We hypothesized that culprit lesion location in the proximal portion of the culprit artery would also be associated with poorer clinical outcomes compared with a mid or distal location. Lesion location and clinical outcomes were evaluated in 2,488 patients from the Thrombolysis In Myocardial Infarction (TIMI) 4, 10A, 10B, and 14 trials. Proximal lesions were located before or at the first major branch of the parent artery, mid lesions were between the first and the second major branches, and all other lesions were classified as distal. Proximal lesions were associated with a higher incidence of in-hospital death or recurrent AMI compared with mid or distal lesions (10.5% [n = 478] vs 6.1% [n = 1,498] vs 3.7% [n = 511], p <0.001), and they were associated with a higher rate of in-hospital death (6.7% [n = 478] vs 3.2% [n = 1,498] vs 2.5% [n = 511], p = 0.001). In a multiple logistic regression model adjusting for TIMI flow grade, age, gender, and pulse, the planimetered distance from the ostium to the LAD culprit lesion was associated with 30-day death or recurrent AMI (odds ratio 0.79 per centimeter increase in distance down the artery, p = 0.01). Proximal culprit lesion location is associated with an increased risk of adverse outcomes after fibrinolytic administration, which is likely due to a larger area of subtended myocardium. In patients with a LAD culprit lesion, proximal lesion location is a multivariate correlate of adverse outcomes even after adjustment for coronary blood flow and other covariates.
The American Journal of Cardiology 10/2003; 92(8):913-8. · 3.37 Impact Factor
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ABSTRACT: We hypothesized that early recurrent myocardial infarction (MI) following fibrinolytic administration would be assessed with higher mortality at both 30 days and 2 years.
Although early recurrent MI after fibrinolytic therapy has been associated with increased early mortality in the acute MI setting, its relation to long-term mortality has not been fully explored.
Mortality data were ascertained in 20,101 patients enrolled in the Thrombolysis In Myocardial Infarction (TIMI) 4, 9, and 10B and Intravenous NPA for the Treatment of Infarcting Myocardium Early (InTIME-II) acute MI trials.
The frequency of symptomatic recurrent MI during the index hospitalization was 4.2% (836/20,101). Recurrent MI during the index hospital period was associated with increased 30-day mortality (16.4% [137/836] vs. 6.2% [1,188/19,260], p < 0.001). Likewise, recurrent MI was associated with a sustained increase in mortality up to two years, even after adjustments were made for covariates known to be associated with mortality and recurrent MI (hazard ratio 2.11, p < 0.001). However, this higher mortality at 2 years was due to an early divergence in mortality by 30 days and was not due to a significant increase in late mortality between 30 days and 2 years (4.38% [31/707] vs. 3.76% [685/18,206], p = NS). Percutaneous coronary intervention during the index hospitalization was associated with a lower rate of in-hospital recurrent MI (1.6% vs. 4.5%, p < 0.001) and lower two-year mortality (5.6% vs. 11.6%, p < 0.001). Performance of coronary artery bypass graft surgery was also associated with a lower recurrent rate of MI (0.7% vs. 4.3%, p < 0.001) and lower two-year mortality rate (7.95% vs. 10.6%, p = 0.0008).
Early recurrent MI is associated with increased mortality up to two years. However, most deaths occur early, and the risk of additional deaths between the index hospital period and two years was not significantly increased among patients with recurrent MI. Percutaneous coronary intervention during the index hospitalization was associated with a lower risk of recurrent MI and a lower risk of two-year mortality.
Journal of the American College of Cardiology 08/2003; 42(1):7-16. · 14.16 Impact Factor
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ABSTRACT: Shorter distances from the coronary ostia to culprit lesions have been associated with a higher incidence of adverse outcomes in ST elevation acute myocardial infarction (STEMI). As drug-eluting stents are associated with low rates of restenosis and formation of a stable intima, we sought to develop a mathematical model to estimate how far down the coronary artery a drug-eluting stent would have to be placed to theoretically mitigate the risk of proximal plaque rupture.
Distances from the ostia to the end of the culprit lesions were planimetered in 1,914 patients from the TIMI 14, INTEGRITI, FASTER and ENTIRE/TIMI 23 trials.
The first 60 mm of the coronary artery contained 75% of STEMI culprit lesions. The median distance from the vessel ostium to the end of the culprit lesion was 43 mm (mean 50 +/- 34) and the relative distance from the vessel ostium to the end of the lesion was 29% (mean 33 +/- 17%) of the total culprit artery length. Diabetes was the only baseline clinical characteristic associated with a longer absolute distance to the end of the culprit lesion (46 mm vs. 43 mm, p = 0.03) as well as relative to total artery length (31% vs. 29%, p = 0.04). Median distances from the artery ostium to the end of the culprit lesion were shortest among the left anterior descending culprits (40 mm), followed by circumflex lesions (43 mm) and then right coronary artery lesions (47 mm, 3-way p < 0.0001).
The majority of culprit lesions in STEMI are contained within the proximal 30% of the major epicardial coronary arteries, but the distance varies depending upon which epicardial artery is involved. Cumulative distribution functions are presented to allow estimation of the percent of culprit lesions lying proximal to any given distance from the ostium to model the feasibility of prophylactic drug-eluting stenting to minimize the risk of subsequent proximal plaque rupture.
Journal of Thrombosis and Thrombolysis 07/2003; 15(3):189-96. · 1.48 Impact Factor
