No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
Is there a relationship between non-obstructive coronary artery disease or cardiac syndrome X and migraine? Αn integrated multi-disciplinary approach
Abstract
Non-obstructive coronary artery disease (CAD) which is mostly called cardiac syndrome X (CSX) is noted in about 30% of men and 40%-60% of women and seems to be incremental. In addition, frequent myocardial perfusion defects with various levels of severity are often seen in this disease. Recently, we noticed that the frequency of migraine in patients with CSX was noticeably higher than in healthy people and in CAD patients. This may support the evolving story that CSX is related to migraine and to chest pain and that CSX and migraine may have a similar pathophysiology. Hence, myocardial perfusion imaging could be used as a complement any diagnostic test to support the relation between CSX and migraine.
ResearchGate has not been able to resolve any citations for this publication.
Cardiac syndrome X (CSX) is defined by an angina-like chest pain, a positive response to stress testing and normal or near normal coronary angiogram. We evaluated the angiographic findings in patients with cardiac syndrome X and compared it with myocardial perfusion scintigraphy findings.
The study included 39 females aged 40-58 years (mean, 49.79 +/- 4.69 [SD] and 13 males ranging from 40 to 54 years (mean, 47.54 +/- 3.76 [SD] with CSX. By reviewing the angiographic film, some variables including stenosis (less than 30% of vessel diameter), delay run off, delay wash out, calcification and tortuosity were evaluated. Thirty-two had been undergone on myocardial perfusion imaging (MPI).
The most frequent abnormal angiographic finding in three territories was stenosis item. Overall, 22 of 32 (68.75%) CSX patients had ischemia on MPI. The result of the myocardial perfusion imaging was not concordant with five angiographic findings.
We suggest that the presence of angiographic coronary findings such as stenosis, delay run off, delay wash out, calcification and tortuosity are not invariably associated with atherosclerosis, and also seen in CSX patients.
Patients with chest pain and no obstructive coronary artery disease (CAD) are considered at low risk for cardiovascular events but evidence supporting this is scarce. We investigated the prognostic implications of stable angina pectoris in relation to the presence and degree of CAD with no obstructive CAD in focus.
We identified 11 223 patients referred for coronary angiography (CAG) in 1998-2009 with stable angina pectoris as indication and 5705 participants from the Copenhagen City Heart Study for comparison. Main outcome measures were major adverse cardiovascular events (MACE), defined as cardiovascular death, myocardial infarction, stroke or heart failure, and all-cause mortality. Significantly more women (65%) than men (32%) had no obstructive CAD (P< 0.001). In Cox's models adjusted for age, body mass index, diabetes, smoking, and use of lipid-lowering or antihypertensive medication, hazard ratios (HRs) associated with no obstructive CAD were similar in men and women. In the pooled analysis, the risk of MACE increased with increasing degrees of CAD with multivariable-adjusted HRs of 1.52 (95% confidence interval, 1.27-1.83) for patients with normal coronary arteries and 1.85 (1.51-2.28) for patients with diffuse non-obstructive CAD compared with the reference population. For all-cause mortality, normal coronary arteries and diffuse non-obstructive CAD were associated with HRs of 1.29 (1.07-1.56) and 1.52 (1.24-1.88), respectively.
Patients with stable angina and normal coronary arteries or diffuse non-obstructive CAD have elevated risks of MACE and all-cause mortality compared with a reference population without ischaemic heart disease.
There is no consensus regarding the definition of cardiac syndrome X (CSX). We systematically reviewed recent literature using a standardized search strategy. We included 57 articles. A total of 47 studies mentioned a male/female distribution. A meta-analysis yielded a pooled proportion of females of 0.56 (n = 1,934 patients, with 95% confidence interval: 0.54-0.59). As much as 9 inclusion criteria and 43 exclusion criteria were found in the 57 articles. Applying these criteria to a population with normal coronary angiograms and treated in 1 year at a general hospital, the attributable CSX incidence varied between 3 and 11%. The many inclusion and exclusion criteria result in a wide range of definitions of CSX and these have large effects on the incidence. This shows the need for a generally accepted definition of CSX.
Cardiac syndrome X is defined by a typical angina pectoris with normal or near normal (stenosis <40%) coronary angiogram with or without electrocardiogram (ECG) change or atypical angina pectoris with normal or near normal coronary angiogram plus a positive none-invasive test (exercise tolerance test or myocardial perfusion scan) with or without ECG change. Studies with myocardial perfusion imaging on this syndrome have indicated some abnormal perfusion scan. We evaluated the role of myocardial perfusion imaging (MPI) and also the severity and extent of perfusion abnormality using Tc-99m MIBI Single Photon Emission Computed Tomography (SPECT) in these patients.
The study group consisted of 36 patients with cardiac syndrome X. The semiquantitative perfusion analysis was performed using exercise Tc-99m MIBI SPECT. The MPI results were analyzed by the number, location and severity of perfusion defects.
Abnormal perfusion defects were detected in 13 (36.10%) cases, while the remaining 23 (63.90%) had normal cardiac imaging. Five of 13 (38.4%) abnormal studies showed multiple perfusion defects. The defects were localized in the apex in 3, apical segments in 4, midventricular segments in 12 and basal segments in 6 cases. Fourteen (56%) of all abnormal segments revealed mild, 7(28%) moderate and 4 (16%) severe reduction of tracer uptake. No fixed defects were identified. The vessel territories were approximately the same in all subjects. The Exercise treadmill test (ETT) was positive in 25(69%) and negative in 11(30%) patients. There was no consistent pattern as related to the extent of MPI defects or exercise test results.
Our study suggests that multiple perfusion abnormalities with different levels of severity are common in cardiac syndrome X, with more than 30 % of these patients having at least one abnormal perfusion segment. Our findings suggest that in these patients microvascular angina is probably more common than is generally believed.
We assessed coronary flow reserve (CFR) by sestamibi imaging in patients with typical chest pain, positive exercise stress test and normal coronary vessels.
Thirty-five patients with typical chest pain and normal angiogram and 12 control subjects with atypical chest pain underwent dipyridamole/rest (99m)Tc-sestamibi imaging. Myocardial blood flow (MBF) was estimated by measuring first transit counts in the pulmonary artery and myocardial counts from SPECT images. Estimated CFR was expressed as the ratio of stress to rest MBF. Rest MBF and CFR were corrected for rate-pressure product (RPP) and expressed as normalised MBF (MBF(n)) and normalised CFR (CFR(n)). Coronary vascular resistances (CVR) were calculated as the ratio between mean arterial pressure and estimated MBF.
At rest, estimated MBF and MBF(n) were lower in controls than in patients (0.98 +/- 0.4 vs 1.30 +/- 0.3 counts/pixel/s and 1.14 +/- 0.5 vs 1.64 +/- 0.6 counts/pixel/s, respectively, both p < 0.02). Stress MBF was not different between controls and patients (2.34 +/- 0.8 vs 2.01 +/- 0.7 counts/pixel/s, p=NS). Estimated CFR was 2.40 +/- 0.3 in controls and 1.54 +/- 0.3 in patients (p < 0.0001). After correction for the RPP, CFR(n) was still higher in controls than in patients (2.1 +/- 0.5 vs 1.29 +/- 0.5, p < 0.0001). At baseline, CVR values were lower (p < 0.01) in patients than in controls. Dipyridamole-induced changes in CVR were greater (p < 0.0001) in controls (-63%) than in patients (-35%). In the overall study population, a significant correlation between dipyridamole-induced changes in CVR and CFR was observed (r = -0.88, p < 0.0001).
SPECT might represent a useful non-invasive method for assessing coronary vascular function in patients with angina and a normal coronary angiogram.
Angiography of patients with typical chest pain reveals normal epicardial coronary arteries in about 20%. Coronary flow reserve (CFR) determination is an elaborate, but helpful, task, as only the evidence of microvascular disease enables appropriate therapy. We prospectively evaluated the incidence of a dysfunctional microcirculation and searched for predictive parameters of a reduced CFR.
In 79 consecutive patients (52 females, 27 males) with typical angina and a normal angiogram and 10 control subjects (6 females, 4 males), CFR was measured by 13N-ammonia rest/dipyridamole PET and correlated with clinical parameters individually and summarized as the number of risk factors (NRF) using an elaborated cardiac risk factor score.
Sixty-five percent of patients had a reduced CFR (CFR < 2.5). CFR correlated with NRF (r = 0.55, P < 0.001), systolic blood pressure (r = 0.46, P < 0.001), interventricular septal thickness (r = 0.33, P < 0.01), and age (r = 0.25, P = 0.02). Eighty-five percent of patients with a high risk factor score (NRF > or = 5) had a reduced CFR. In contrast, 100% of our patients with a low risk factor score (NRF < 2) presented a normal CFR. In total, 55% of our patients could be allocated to either one of these groups.
In about two thirds of patients, anginal pain can be explained by a reduced CFR. Risk factors have a cumulative negative effect on CFR. A clinical cardiac risk factor analysis enables estimation of individual probability of microvascular dysfunction in a significant proportion of these patients. However, CFR measurements are recommended for those with an intermediate NRF.
(1) To identify myocardial perfusion abnormalities in a cohort of patients having coronary artery disease (CAD) risk factors, with either suspected or clinical evidence of ischaemic heart disease (IHD), and with varying degree of coronary artery stenosis. (2) To evaluate the clinical significance of the extent and severity of perfusion abnormalities assessed by myocardial perfusion scintigraphy (MPS) in relation to the anatomical location of coronary stenosis demonstrated by five-vessel selective coronary angiography (SCA).
One hundred and thirty-eight patients (106 male, 32 female) with suspected or clinical evidence of IHD underwent diagnostic evaluation at the Central Hospital of Nicosia, between November 2002 and August 2003. The diagnostic work-up included clinical examination, exercise tolerance test, SCA and myocardial perfusion scintigraphy (MPS) using either Tl chloride or Tc-tetrofosmin.
Based on the results of SCA, patients were divided into five groups on the basis of stenosis as cross-sectional area of coronary artery lumen and its haemodynamic significance, ranging from group 1=less than 50% coronary stenosis to group 5=100% stenosis (occlusion). Nine of 11 (40.9%) patients with angiographically normal coronary arteries (group 1) had moderate inducible reversible ischaemia on MPS and 9/47 (19.1%) patients with insignificant coronary stenosis (less than 75% stenosis=group 2) had fixed perfusion defects, compatible with previous myocardial infarction. The extent of perfusion abnormalities in post-stress MPS patients from group 2 was not found to be statistically significant (P>0.05) when compared to patients belonging to groups 3, 4 and 5. However, the extent of perfusion abnormalities between patients from group 2, when compared to groups 3, 4 and 5 demonstrated significant statistical difference (P<0.05) on post-rest MPS studies. Furthermore, there was no significant statistical correlation between anatomical location of coronary stenosis and severity of perfusion abnormalities in the corresponding myocardial segments.
Patients with CAD risk factors, and coronary arteries with insignificant stenosis on angiography, may demonstrate inducible reversible myocardial ischaemia. This is suggestive of coronary endothelial dysfunction. Patients with insignificant coronary artery stenosis and no previous history of adverse coronary events may demonstrate features of previous myocardial infarction on MPS. The severity of perfusion defects demonstrated by MPS may be independent of the anatomical location of coronary artery stenosis.
The Precision Medicine Initiative recently announced by President Barack Obama seeks to move the field of precision medicine more rapidly into clinical care. Precision medicine revolves around the concept of integrating individual-level data including genomics, biomarkers, lifestyle and other environmental factors, wearable device physiological data, and information from electronic health records to ultimately provide better clinical care to individual patients. The Precision Medicine Initiative as currently structured will primarily fund efforts in cancer genomics with longer-term goals of advancing precision medicine to all areas of health, and will be supported through creation of a 1 million person cohort study across the United States. This focused effort on precision medicine provides scientists, clinicians, and patients within the cardiovascular community an opportunity to work together boldly to advance clinical care; the community needs to be aware and engaged in the process as it progresses. This article provides a framework for potential involvement of the cardiovascular community in the Precision Medicine Initiative, while highlighting significant challenges for its successful implementation.
Recognition of ischemic heart disease (IHD) is often delayed or deferred in women. Thus, many at risk for adverse outcomes are not provided specific diagnostic, preventive, and/or treatment strategies. This lack of recognition is related to sex-specific IHD pathophysiology that differs from traditional models using data from men with flow-limiting coronary artery disease (CAD) obstructions. Symptomatic women are less likely to have obstructive CAD than men with similar symptoms, and tend to have coronary microvascular dysfunction, plaque erosion, and thrombus formation. Emerging data document that more extensive, nonobstructive CAD involvement, hypertension, and diabetes are associated with major adverse events similar to those with obstructive CAD. A central emerging paradigm is the concept of nonobstructive CAD as a cause of IHD and related adverse outcomes among women. This position paper summarizes currently available knowledge and gaps in that knowledge, and recommends management options that could be useful until additional evidence emerges.
![Graphic][1]
An ever-growing number of studies and editorials herald the promise of ‘precision medicine’. On the diagnostic side, new technologies and analytical tools will allow us to pinpoint patient-specific differences and on the treatment-side novel therapies will permit us to exploit those differences for better outcomes.
A combination of genomic, epigenomic, transcriptomic, and metabolomics information—a patient's ‘panomic’ data—may soon be part of an individual medical record. And innovative therapies such as ivacaftor, a cystic fibrosis treatment that targets only a small set of mutations in the CFTR gene, could be weapons in our treatment armamentarium to provide the ‘right drug in the right dose at the right time’.
When US President Barack Obama spotlighted such opportunities by launching his new Precision Medicine Initiative in January 2015, he focused upon opportunities in cancer and diabetes. How will precision medicine fit into cardiology?
Advances in precision medicine will likely accrue to cardiology rapidly. While our field was not a focus of the initial excitement surrounding the Precision Medicine Initiative announcement, I believe cardiology is poised to be a leader in the development of this discipline, based upon more than half a century of contributions. Indeed, the pioneering Framingham Study was instrumental in introducing the concept of disease prediction based upon patient-specific data or ‘factors of risk’—serum cholesterol and blood pressure.5 Large randomized clinical trials, another innovation grounded in cardiology, provided additional datasets mined for …
[1]: /embed/inline-graphic-1.gif
Among angina patients undergoing coronary angiography to further evaluate suspected ischemic heart disease (IHD), "normal" or "non-obstructive" coronary artery disease (CAD) is found in 30% of men and 40-60% of women and appears to be increasing.(1) It is becoming very clear that such patients do not have benign outcomes as documented in larger and larger prospective cohorts.(2-5) Also important are accumulating data indicating that patient-reported outcomes and societal implications rival those observed with obstructive CAD.(6, 7.)
Chest pain is an alarming symptom; it justifies many visits to the emergency department (ED). The etiology is often unknown. Chest wall pain in the presence of migraine headache, although not a common occurrence, is intriguing when it resolves with antimigraine treatment.
To characterize the manifestations and outcomes and investigate the relationship between chest wall pain and headache as a manifestation of migraine exacerbation.
Among patients visiting our ED, we identified those individuals whose pain originated in the chest wall in the setting of migraine exacerbation. Patients with clinical indications for specific treatments were dispositioned accordingly. Control of symptoms including chest pain and headache with antimigraine agents was considered the primary outcome. A prospective follow-up via telephone interview and medical records review was performed.
We collected a convenience sample of 33 patients. All manifested migraine headache with an earlier onset than the chest pain, and all had taken medications prior to visiting the ED. Twelve patients reported a higher visual analog scale score for the headache than for the chest pain. Still, chest pain was the main complaint. The chest pain originated at the chest wall. Ten patients received sublingual nitroglycerin or opiates, or both; no pain relief was reported. However, all symptoms resolved with metoclopramide. On follow-up, 6 patients reported recurrence of chest pain with subsequent migraines.
Chest pain can be a complication of migraine. The treatment should be focused on migraine control. Migraine should be included in the differential diagnosis of chest pain.
Aim To define the prognostic impact of stress myocardial perfusion scintigraphy (MPS) in patients with angiographic exclusion of significant coronary artery disease.
Methods Angiographic and MPS databases were matched to define patients without significant coronary artery disease by quantitative angiography (diameter stenosis <50%) who underwent stress MPS and coronary angiography within a time period of 3 months. A total of 118 patients were identified and followed for a mean of 6.3 ± 1.2 years for death, a composite of death, myocardial infarction, bypass surgery, or percutaneous coronary intervention [MAE]) as well as occurrence of symptoms (angina or dyspnoe class CCS II to IV). Stress and rest MPS (using 99mTc-MIBI or tetrofosmin) were analyzed by quantitative perfusion SPECT (QPS) for summed stress and rest scores (SSS/SRS).
Results There were 16 deaths, 29 MAE, and 76 patients with MAE or significant symptoms during follow-up. Significant differences in SSS were found between patients who died (9.5 ± 6.9 vs. 5.4 ± 5.6, P = 0.012), had MAE (8.7 ± 7.2 vs. 5.2 ± 5.0, P = 0.010), or had MAE or significant clinical symptoms (7.2 ± 7.1 vs. 4.6 ± 6.2, P = 0.042) compared to those without the respective event. Logistic regression analysis demonstrated SSS to be a predictor of death (OR = 1.074 [95% CI: 1.004-1.149], P = 0.026) and MAE (OR = 1.087 [95% CI: 1.004-1.181], P = 0.027).
Conclusions In patients without significant angiographic coronary artery disease, the result of stress MPS is a predictor of long-term prognosis. Quantitative analysis of MPS allows definition of patients with a higher likelihood to develop clinical events or symptoms.
Myocardial perfusion single-photon emission computed tomography (SPECT) has been extensively applied in the clinical assessment of patients with diabetes mellitus. The aim of the present study was to evaluate stress technetium-99m sestamibi SPECT MPI perfusion in silent myocardial ischemia and its association with some clinical and laboratory parameters in an asymptomatic diabetic population.
83 subjects (age: 57.1±6.9 years) with at least five years history of type 2 diabetes, and no suspected or documented coronary artery disease (CAD) accomplished myocardial perfusion imaging; angiography was also performed in patients with abnormal MPI.
MPI results showed that 58 patients had normal myocardial perfusion, while 25 patients showed perfusion defects (23 reversible and 2 fixed) on MPI. 12 out of the 25 (48%) with abnormal MPI findings represented abnormal angiography. We observed that pretest likelihood of CAD (odds ratio 2.32; 95%-CI: 1.05-5.13; p = 0.038) and higher HbA1c level (odds ratio 1.70; 95%-CI, 1.07-2.71; p = 0.02) were independently associated with abnormal MPI.
Occult CAD was present on MPI in 1/3 patients with DM without abnormal electrocardiographic findings or evidence of peripheral arterial disease.
The diagnosis of cardiac syndrome X (CSX) is often a diagnosis of exclusion and hence requires a systematic and comprehensive assessment of each patient to rule out more common causes of chest discomfort. The definitive technique for the diagnosis of CSX is not currently available. Many patients with chest pain and normal coronary angiograms have neither metabolic nor hemodynamic evidence of myocardial ischemia. Causes of nonischemic chest pain such as esophageal dysfunction, pulmonary hypertension, and mitral valve prolapse, should also be considered and pursued. Although chronic inflammation induced by Helicobacter pylori infection might play a part in the pathophysiology of CSX, one can conclude that nonischemic chest pain resulting from gastrointestinal disease such as esophagitis, gastritis cannot be completely excluded in the patients with CSX. We believe future large scale prospective cohort studies will be needed to solve that dilemma.
A subset of subjects undergoing myocardial perfusion imaging has perfusion abnormalities that are subsequently labeled false positive based on coronary angiography. We evaluated the long-term prevalence of cardiovascular events in these patients. We retrospectively identified 48 patients who had reversible perfusion abnormalities with myocardial perfusion imaging and normal coronary angiography. Patients with known coronary artery disease, left ventricular dysfunction, valvular disease, and cardiomyopathy were excluded. Patient follow-up, conducted for at least 3 (mean interval, 7.4) years from the index myocardial perfusion imaging, was accomplished by a review of medical records and telephone interviews. Study endpoints were cardiovascular events defined as sudden cardiac death, myocardial infarction, percutaneous coronary revascularization, coronary artery bypass grafting, and cerebrovascular or peripheral revascularization. Thirty-one percent (15 of 48) of the patients had cardiovascular events. Six of the 48 patients had coronary events. These patients had abnormal myocardial perfusion imaging and normal coronary angiogram. The time between myocardial perfusion imaging and coronary event was 0.5 to 8.67 years. There was a strong correlation between the regions of original perfusion abnormality and the ultimate coronary ischemia or revascularization. Abnormal findings on myocardial perfusion imaging may predict a higher prevalence of coronary and peripheral vascular events than suggested by a normal coronary angiogram.
Migraine headaches have rarely been associated with a disturbance of the cardiovascular system. This report describes a clinical syndrome encountered in twelve patients, characterized by classical migraine headaches, chest pain and symptomatic functional hypoglycemia. Attention is called to the possible role that coronary spasm may play in the cause of chest pain. The author speculates a possible interrelationship between migraine headache, coronary spasm and myocardial infarction.
It remains unclear whether myocardial ischemia due to coronary microvascular dysfunction is the cause of chest pain in syndrome X (chest pain, ischemic-like stress ECG despite angiographically normal coronary arteries). To assess the function of the coronary microcirculation and its relation to pain perception, we measured myocardial blood flow (MBF) and coronary vasodilator reserve (CVR) in 29 patients with syndrome X and 20 matched normal control subjects.
MBF at rest and after intravenous dipyridamole (0.56 mg.kg-1 over 4 minutes) was measured using positron emission tomography with H2(15)O. CVR was calculated as MBFdipyridamole/MBFrest. ECG changes and chest pain after dipyridamole in syndrome X were compared with those in 35 patients with coronary artery disease (CAD). Resting and postdipyridamole MBFs were homogeneous throughout the left ventricle in syndrome X patients and control subjects. MBF was 1.05 (0.25), mean (SD) versus 1.00 (0.22) mL.min-1.g-1 (P = NS) at rest and 2.73 (0.81) versus 3.00 (1.00) mL.min-1.g-1 (P = NS) after dipyridamole in patients and control subjects, respectively. CVRs were 2.66 (0.76) and 3.06 (1.08) (P = NS) and after correction of resting MBF for rate-pressure product were 2.35 (0.83) and 2.34 (0.90) (P = NS) in patients and control subjects, respectively. Female syndrome X patients had higher resting MBF than males, at 1.18 (0.20) versus 0.88 (0.19) mL.min-1.g-1 (P < .001). Chest pain after dipyridamole occurred in syndrome X as frequently as in CAD (21/29 versus 22/35, P = NS).
When patients with syndrome X are compared with control subjects, no differences are found in MBF either at rest or after dipyridamole, despite syndrome X patients experiencing chest pain after dipyridamole to the same extent as patients with CAD. These findings, together with the absence of any relation among MBF, chest pain, and ECG changes under stress, cast further doubt on ischemia as the basis of the chest pain, at least in the majority of syndrome X patients.
Myocardial blood flow (MBF) was measured using continuous inhalation of oxygen-15-labeled carbon dioxide, and positron emission tomography before and after intravenous dipyridamole in 13 patients with syndrome X (angina pectoris, angiographically normal coronary arteries, positive exercise test and negative ergonovine test), 7 healthy subjects and 8 patients with 1-vessel coronary artery disease (CAD). In patients with syndrome X, baseline MBF was greater than in healthy subjects and patients with CAD (1.24 +/- 0.27 vs 0.87 +/- 0.07 and 1.03 +/- 0.23 ml/g/min, respectively; p < 0.05), and more heterogeneous (34 +/- 7 vs 26 +/- 5 and 25 +/- 6, respectively; p < 0.05) as assessed by the coefficient of variation among myocardial regions < or = 2.3 cm3. After dipyridamole, MBF in patients with syndrome X was similar to that in healthy subjects (2.95 +/- 0.75 vs 3.40 +/- 0.82 ml/g/min; p = NS) and greater than in patients with CAD (1.78 +/- 0.76 ml/g/min; p < 0.05). However in patients with both syndrome X and CAD, MBF was more heterogeneous than in healthy subjects (48 +/- 12 and 48 +/- 11, respectively, vs 30 +/- 7; p < 0.01). Thus, in patients with syndrome X, MBF is abnormally heterogeneous both at baseline and after dipyridamole. These findings are compatible with the presence of dynamic alterations of small coronary arteries. Because these alterations appear to be very sparse within the myocardium, they can be undetected when myocardial perfusion, function and metabolism are assessed using conventional methods that are unable to detect small myocardial regions.
Single-photon emission computed tomography (SPECT) sestamibi (MIBI) is an excellent tool for detection of coronary artery disease (CAD), preoperative risk assessment, and follow-up management after coronary revascularization. While the sensitivity of MIBI SPECT for detecting CAD has been reported to exceed 90%, the specificity ranges between 53-100%.
The study was undertaken to assess characteristics of patients with abnormal stress technetium Tc99m sestamibi SPECT (MIBI) studies without significant coronary artery diameter stenoses (< 50%).
Between January 1999 and November 2000, 270 consecutive patients were referred for coronary angiography due to reversible MIBI uptake defects during exercise. In 41 patients (15%; 39% women, mean age 59 +/- 9 years), reversible MIBI uptake defects were assessed although coronary angiography showed no significant CAD. These patients were compared with age- and gender-matched patients with perfusion abnormalities (39% women, mean age 60 +/- 9 years), due to significant CAD (coronary artery stenosis > 50%).
There were no significant differences between the two groups regarding body mass index, left bundle-branch block (LBBB), or method of stress test (dipyridamole in patients with LBBB or physical inactivity [n = 11] and exercise in all the others [n = 30]). Left ventricular hypertrophy (44 vs. 23%, p = 0.05) and left anterior fascicular block (LAFB) (17 vs. 0%, p = 0.005) were more common in patients with perfusion abnormalities with no significant CAD, whereas ST-segment depression during exercise (17 vs. 37% p = 0.05) and angina during exercise (15 vs. 29%, p = 0.02) were significantly less common than in patients with abnormal MIBI perfusion studies and angiographically significant CAD. Sestamibi uptake defects during exercise were significantly smaller in patients without significant CAD than in matched controls with significant CAD (p < 0.0004).
Of 270 consecutive patients, 41 (15%) referred to coronary angiography due to reversible MIBI uptake defects showed coronary artery stenoses < 50%. Twenty-six (10%) of these presented angiographically normal coronary arteries. The significantly higher proportion of left ventricular hypertrophy and LAFB in patients with reversible MIBI uptake defects without significant CAD suggest microvascular disease, angiographically underestimated CAD, and conduction abnormalities as underlying mechanisms.
To examine the association between a lifetime history of migraines and other headaches with and without aura and Rose angina and coronary heart disease (CHD).
Participants were 12,409 African American and white men and women from the Atherosclerosis Risk in Communities Study, categorized by their lifetime history of headaches lasting > or =4 hours (migraine with aura, migraine without aura, other headaches with aura, other headaches without aura, no headaches). Gender-specific associations of headaches with Rose angina and CHD, adjusted for sociodemographic and cardiovascular disease risk factors, were evaluated using Poisson regression.
Participants with a history of migraines and other headaches were more likely to have a history of Rose angina than those without headaches. The associations were stronger for migraine and other headaches with aura (prevalence ratio [PR] = 3.0, 95% CI = 2.4, 3.7 and PR = 2.0, 95% CI = 1.5, 2.7 for women; PR = 2.2, 95% CI = 1.2, 3.9 and PR = 2.4, 95% CI = 1.4, 3.9 for men) than for migraine and other headaches without aura (PR = 1.5, 95% CI = 1.2, 1.9 and PR = 1.3, 95% CI = 1.1, 1.6 for women; PR = 1.9, 95% CI = 1.2, 2.9 and OR = 1.4, 95% CI = 1.0, 1.8 for men). In contrast, migraine and other headaches were not associated with CHD, regardless of the presence of aura.
The lack of association of migraines with coronary heart disease suggests that the association of migraine with Rose angina is not related to coronary artery disease. Future research assessing other common underlying pathologic mechanisms is warranted.
There are conflicting data regarding the association between migraines and cardiovascular events. We evaluated the relationship between migraine headaches, angiographic coronary artery disease, and cardiovascular events in women.
The Women's Ischemia Syndrome Evaluation (WISE) study is a National Heart, Lung and Blood Institute (NHLBI)-sponsored prospective, multicenter study aiming to improve ischemia evaluation in women. A total of 944 women presenting with chest pain or symptoms suggestive of myocardial ischemia were enrolled and underwent complete demographic, medical, and psychosocial history, physical examination, and coronary angiography testing. A smaller subset of 905 women, representing a mean age of 58 years, answered questions regarding a history of migraines. We prospectively followed 873 women for 4.4 years for cardiovascular events and all-cause mortality.
Women reporting a history of migraines (n=220) had lower angiographic coronary severity scores, and less severe (> or = 70% luminal stenosis) angiographic coronary artery disease compared to women without a history of migraines (n=685). These differences remained statistically significant after adjustment for age and other important cardiac risk factors. On prospective follow-up of a median of 4.4 years, women with a history of migraines were not more likely to have a cardiovascular event (hazard ratio [HR] 1.2; 95% confidence interval [CI], 0.93-1.58) and migraines did not predict all-cause mortality (HR 0.96; 95% CI, 0.49-1.99).
Among women undergoing coronary angiography for suspected ischemia, those reporting migraines had less severe angiographic coronary artery disease. We could not support an association between migraines and cardiovascular events or death. Further research studying the common pathophysiology underlying migraines and cardiovascular disease is warranted.
The purpose of this study was to investigate whether endothelial dysfunction contributes to abnormal myocardial perfusion imaging (MPI) observed in patients without obstructive coronary artery disease (CAD). It is unclear whether reversible MPI defects detected in the absence of obstructive CAD represent underlying vascular pathology or are false-positive MPI results. Recent evidence suggests that coronary endothelial dysfunction might play a role in the pathogenesis of these defects.
We prospectively recruited 36 patients with chest discomfort, reversible abnormalities on MPI, and nonobstructive or absent CAD (stenosis <50% on coronary angiography). The control group (n = 55) consisted of patients with chest discomfort and similar cardiac risk factors but with normal MPI findings. Vascular endothelial function was assessed in the brachial artery by ultrasound as the response to hyperemia and reported as percent flow-mediated dilation (FMD). Response to sublingual nitroglycerin was used as an indicator of endothelium-independent vasodilation. The patients with abnormal MPI findings and nonobstructive CAD had a significantly lower FMD (9.0% +/- 7.2%), indicating endothelial dysfunction, compared with those with similar risk factors and normal MPI findings (12% +/- 5.2%) (P = .03). Baseline brachial artery size and endothelium-independent dilation were similar between groups. On multivariate analysis, only endothelial dysfunction was predictive of reversible MPI defects.
Patients with chest pain and reversible MPI defects but without obstructive CAD have lower FMD indicative of endothelial dysfunction, as compared with similar patients with normal MPI findings. The possibility of a causal link between reversible MPI defects and endothelial dysfunction needs further exploration.
Cardiac syndrome X is defined by an angina pectoris with normal or near normal coronary angiogram.We evaluated the association of Helicobacter pylori (HP) infection with cardiac syndrome X (CSX). We studied 30 patients with CSX, 30 cases with stable angina and also 30 healthy controls. All three groups underwent urea breath test (UBT). Fifty percent (15 out of 30) of CSX patients had positive UBT result (> or =200 dpm), while two other groups did not have the positive results. Regarding high prevalence of HP infection in patients with CSX in our study and probable causative effect of chronic infection in coronary artery diseases, possible role of HP infection in the pathogenesis of CSX is suggested. However well designed clinical trial studies are needed to confirm this preliminary result.
In the absence of significant coronary stenoses, stress-induced myocardial perfusion abnormalities at gated single photon emission computed tomography (g-SPECT) are usually considered to be a 'false-positive' result. Our goal was to investigate how false-positive g-SPECT perfusion abnormalities relate to cardiovascular risk factors and whether they provide any prognostic information.
From 1999 to 2005, a group of 130 anginal patients with myocardial perfusion abnormalities at stress g-SPECT, with normal coronary angiography or less than 50% lumen reduction and with a left ventricular ejection fraction more than 0.45, was selected. The extent of myocardial perfusion abnormalities after stress was quantified using the summed difference score (SDS).
Using a logistic regression model, it was found that cardiovascular risk factors (diabetes mellitus, arterial hypertension, smoking habit, hypercholesterolemia and obesity) were closely related (r = 0.96) to the SDS. During a 44 +/- 7-month follow-up, six patients experienced nonfatal cardiac events. An SDS more than 7 (P < 0.0001) and diabetes mellitus (P < 0.0001) were the only independent predictors of event-free survival using Cox proportional hazard regression analysis.
In patients with anginal-like chest pain and without significant coronary stenoses, stress-induced myocardial perfusion abnormalities at g-SPECT correlate with cardiovascular risk factors and are independent predictors of the few, minor adverse cardiac events during the follow-up.
- S Agrawal
- P K Mehta
Agrawal S, Mehta PK, Bairey Merz CN. Cardiac Syndrome X: Update.
Heart Failure Clinics 2016; 12: 141-56.
The Achilles heel of SPECT imaging: the false-positive scans-or are they? J Nucl Cardiol: o cial publication of the American Society of
- A E Iskandrian
Iskandrian AE. The Achilles heel of SPECT imaging: the false-positive scans-or are they? J Nucl Cardiol: o cial publication of the
American Society of Nuclear Cardiology 2006; 13: 747-8.
Imaging in the Age of Precision Medicine
- C J Herold
- J S Lewin
- A G Wibmer
Herold CJ, Lewin JS, Wibmer AG, et al. Imaging in the Age of Precision Medicine: Summary of the Proceedings of the 10th Biannual
Symposium of the International Society for Strategic Studies in
Radiology. Radiology 2016; 279: 226-38.