Coronary vasospasm: is it a myth?

This review addresses some myths about coronary vasospasm as the cause of angina pectoris. Coronary artery vasospasm is a common phenomenon, which is clinically encountered by busy cardiologists almost on a daily basis. It is the cause of resting angina in many patients without significant coronary artery disease, but also in patients with atherosclerotic coronary artery disease but no subtotal lesion. Although coronary artery vasospasm can be suspected clinically, proof cannot usually be obtained by non-invasive means but is easily available during cardiac catheterization. Patients with vasospastic angina are repeatedly exposed to this invasive procedure as most cardiologists suspect a coronary lesion requiring intervention as the cause of the patient's resting angina. Adding an intracoronary acetylcholine test to the catheterization procedure may establish the correct diagnosis and enable treatment with calcium antagonists and nitrates. Epicardial vasospasm may be observed during the test in patients with and without angiographically visible lesions in the coronary arteries. Almost 50% of all pathological tests, however, do not show epicardial vasospasm but reproduction of symptoms and electrocardiogram signs of ischemia indicating spasm of the microvessels.

Diagnostic synergy of non-invasive cardiovascular magnetic resonance and invasive endomyocardial biopsy in troponin-positive patients without coronary artery disease.

AIMS: Only few data are available regarding a direct comparison of both non-invasive CMR and invasive EMB with respect to conformity of procedure-derived diagnoses in the same patients. The aim of this study was to elucidate the diagnostic performance of non-invasive cardiovascular magnetic resonance imaging (CMR) and endomyocardial biopsy (EMB) in patients with troponin-I (TnI) positive acute chest pain in the absence of significant coronary artery disease (CAD). METHODS AND RESULTS: One thousand one hundred and seventy-four consecutive patients who were admitted with TnI-positive acute chest pain between March 2004 and July 2007 underwent coronary angiography. In 1012 patients (86%), significant CAD (stenosis >50%) was detected as underlying reason for the acute chest pain. In 82 out of the remaining 162 patients without significant CAD, further workup was performed including both CMR and EMB. Cardiovascular magnetic resonance imaging alone enabled a diagnosis in 66/82 (80%) and EMB alone in 72/82 (88%) patients (P = 0.31). Myocarditis was the most frequent diagnosis by both CMR and EMB in this cohort and was detected with a higher frequency by EMB (58 vs. 81%; P < 0.001). With the combined approach comprising CMR and EMB, a final diagnosis could be established applying the 'Believe-The-Positive-Rule' in 78/82 patients (95%). This combined approach turned out to yield more diagnoses than either CMR (P < 0.001) or EMB (P = 0.03) as single techniques, respectively. Comparison of diagnostic CMR procedures with the corresponding diagnostic EMBs demonstrated a substantial match of diagnoses (kappa = 0.70). CONCLUSION: Cardiovascular magnetic resonance imaging and EMB have good diagnostic performances as single techniques in patients with TnI-positive acute chest pain in the absence of CAD. The combined application of CMR and EMB yields a considerable diagnostic synergy by overcoming some limitations of CMR and EMB as individually applied techniques.

Caucasian patients suffering from coronary vasospastic angina have an intact peripheral endothelium-dependent vasoreactivity.

We sought to evaluate whether Caucasian patients suffering from vasospastic angina have a decreased brachial artery flow-mediated dilation (FMD) like their Japanese counterparts and whether certain serum factors known to be associated with impaired vasomotility or endothelial dysfunction are abnormal. In this prospectively conducted study, 33 subjects presenting with resting angina were identified to suffer from coronary vasospastic angina (coronary spasm group). A control group of 19 subjects with matched cardiovascular risk profiles was defined out of patients admitted to our hospital for evaluation of atypical chest pain. Intracoronary acetylcholine(ACh)-testing for vasospasm was performed in all patients after coronary artery disease (CAD) had been ruled out. Brachial artery FMD was measured using high-resolution ultrasound. There was no significant difference in brachial artery FMD between the coronary spasm and the control group (7.05+/-2.24% vs. 7.12+/-2.50%; p=0.93). The endothelium-independent vasodilator response of the brachial artery to sublingual nitroglycerin did not differ either between the two groups (21.88+/-6.13% vs. 21.48+/-7.38%; p=0.84). Simple and multiple linear regression analysis revealed that only baseline brachial artery diameter was a significant determinant of FMD (p<0.0001). No relationship could be detected between impaired coronary vasomotility and peripheral endothelium-dependent or independent vasodilation in Caucasian patients suffering from coronary vasospastic angina illustrating a further clue for racial differences in the pathophysiology of vasospastic angina.