Limitations of Medical Therapy in Patients With Pure Coronary Spastic Angina*

Seung

et al. 2007

Circ J

lthough acute myocardial infarction (AMI) is mostly associated with obstructive coronary artery disease, myocardial infarction with normal epicardial coronary arteries has been documented. [1][2][3][4][5] The overall prevalence of myocardial infarction (MI) with a normal coronary angiogram is low, approximately 3%, but the incidence of this condition appears to vary with age, with higher rates in younger patients. 4,5 In some patients with a diagnosis of vasospastic angina (VA), dangerous complications such as AMI, or a high-degree of atrioventricular block, ventricular tachycardia, fibrillation or electromechanical dissociation, are observed during an ischemic attack, and all of these maladies can lead to sudden death. Coronary artery spasm has been proposed as a classic etiologic factors for AMI with normal coronary arteries, 6 but the actual prevalence of this event has remained ill-defined because of a lack of data from spasm provocation tests in a large series of patients.In the present study we evaluated the clinical and angiographic characteristics of VA with AMI in patients without organic coronary heart disease. Circulation Journal Vol.71, September 2007 Methods PatientsBetween January 2003 and June 2005, 672 coronary spasm provocation tests were performed at Kangnam St Mary's hospital and 292 patients were diagnosed with VA. Among these 292 patients, 21 had an AMI. In this study, the diagnosis of VA was made when patients met all of the following criteria: (1) burning or squeezing retrosternal chest pain, (2) positive spasm provocation test, and (3) no significant organic lesion (<50% narrowing of the coronary luminal diameter according to quantitative coronary angiography (QCA)). AMI with VA was defined by elevation of the cardiac markers (troponin-I >upper normal limit and creatine kinase-MB >3-fold the upper normal limit) with no organic coronary heart disease being identified on angiography. We excluded patients with takotsubo cardiomyopathy.After the procedure was explained, written informed consent for the spasm provocation test was given by all the patients. Spasm Provocation TestAll the patients' medications, except for nitroglycerin, were discontinued for >48 h before the start of the study, and nitroglycerin was discontinued at least >4 h before the start of the study. Cardiac catheterization was performed through the right femoral artery while the patient was in a fasting state. Control angiograms of the left coronary artery (LCA) were obtained in the right anterior oblique view with caudal projection, before imaging of the right coronary artery (RCA) in the left anterior oblique view with straight projection after the injection of 4-6 ml of contrast medium.Circ J 2007; 71: 1383 -1386 (Received June 7, 2006 revised manuscript received April 6, 2007; accepted May 24, 2007 There were 20 patients who initially visited the emergency room for AMI without suffering prior VA. One patient with a history of VA had an AMI when he discontinued his medication. Among the 21 VA patients with AMI, 14 ha...

Section: Angiographic Analysismentioning

confidence: 99%

Clinical and Angiographic Characteristics of Acute Myocardial Infarction Caused by Vasospastic Angina Without Organic Coronary Heart Disease

Seung

et al. 2007

Circ J

“…However, resistance to calcium channel blockers is frequent [15], which may require the combination of nitrate derivatives or equivalents.…”

Section: Discussionmentioning

confidence: 99%

Prinzmetal or Vasospastic Angina in a Young Woman: An Under-Diagnosed Pathology

Js¹,

Dioum²,

Mb³

et al. 2017

J Clin Exp Cardiolog

Vasospastic angina is considered rare but its prevalence is probably underestimated, especially in the case of atheromatous coronary lesions. Its diagnosis remains important because of its poor prognosis and its therapeutic features. We report a clinical case illustrating the issue of vasospastic angina's diagnosis. Diagnostic ways such as coronary spasm challenge tests must be adapted to the evolution of the techniques and the use of coronary angiography nowadays, in particular the preferential use of the radial pathway especially in women with a smaller radial caliber compared to men. Clinical CaseWe report through this clinical observation the issue of the diagnosis of vasospastic angina or Prinzmetal's angina (VSA).Mrs. GV, 41 years old, had as a cardiovascular risk factor an active smoking at the rate of 15 packs-year and a family history of coronary heart disease. She was admitted to the emergency department for a stable angina evolving for three weeks with episodes at rest.Biology noted an elevation of ultra-sensitive troponins to 220 ng/l. The electrocardiogram was normal, echocardiography noted moderate hypokinesis of left ventricle contractility in apical anterior, apex and anterior territories.The coronary angiography performed by right radial artery access with a 5 french catheter concluded to intermediate coronary lesions at 50% in the distal part of the left main coronary artery (LMCA), encompassing the origin of the left circumflex artery (LCA) and left anterior descending artery or LAD (Classification Medina 1-0-0), and a lesion of 50% in the distal portion of the middle right coronary artery or RCA (Figures 1 and 2).The measurement of the coronary reserve by Fractional Flow Reserve [FFR] towards the three axes was respectively 0.82 to the LAD, 0.83 to the circumflex artery and 0.92 to the right coronary artery.Drug therapy including beta-blockers, aspirin, clopidogrel, statins and a nitroglycerin transdermal patch was initiated. The patient was advised on the need for good control of cardiovascular risk factors, specially smoking cessation.Three days later, she presented a new recurrence of identical chest pain that occurred at rest for 10 minutes, leading her back to the emergency room.At rest, the electrocardiogram showed electrical modifications like repolarization disorders of biphasic T-type in V1 and V2 precordial leads; getting normal on the following electrocardiograms. Troponins were increased to 327 ng/l.The control coronary angiography performed again by the right radial artery access without injection of vasodilator, did not find an evaluative lesion. The methylergometrine testing was positive with the reappearance of chest pain, T-wave negativity in V1 lead (Figure 3) and spastic occlusion of the proximal LAD (Figure 4), regressive after intra-coronary injection of 3 milligrams of isosorbide dinitrate (Figures 5 and 6).

“…43,44) The success with these 2 classes of agents either alone or in combination has minimized the necessity for additional therapeutic approaches. However, a recent report by Sueda et al 45) suggested that calcium 7 CORONARY SPASM channel blockers may not be as effective as previously determined because only 38% of patients on long -acting calcium channel blockers had complete resolution of symptoms. In addition to this therapeutic concern, a certain number of patients cannot tolerate these agents, and alternative approaches are required.…”

Section: Therapeutic Approachmentioning

confidence: 91%

Mechanistic Insights of Coronary Vasospasm and New Therapeutic Approaches

Saitoh

Takeishi

Maruyama

2015

FJMS

PREFACECoronary vasospasm is a major health problem in Japan because of its high incidence and severity. Great advances have been made in clinical research and therapy focusing on coronary vasospastic angina. In particular, the Ca antagonist has contributed to improvements in the quality of life of patients with coronary vasospastic angina. Moreover, several animal models of coronary vasospasm have provided insight into the pathophysiology of this disease. However, the mechanisms of coronary vasospasm and microvascular spasm remain elusive. We have studied the mechanisms of coronary vasospasm, including microvascular spasm, in an animal model. The present study was designed to develop an animal model of coronary vasospasm and to elucidate the mechanisms and pathophysiology of coronary vasospasm and new therapeutic approaches. The topics discussed in this article include : (1) the role of endothelial and smooth muscle function on the genesis of coronary vasospasm, (2) the participation of reactive oxygen species in coronary vasospasm, and (3) aging and spasm. We hope that the contents of this volume will be useful to "students of coronary vasospasm" at many levels, including the clinician involved in cardiovascular studies and scientists in various disciplines who are interested in a comprehensive, in -depth review of coronary vasospasm.Coronary vasospasm can be defined as a reversible, focal, and intense coronary vasoconstriction that typically occurs in an epicardial conduit artery segment. The definitive diagnosis of a coronary artery spasm is determined by the direct visualization of such a reversible focal subtotal coronary occlusion at a site distal to the catheter tip. This is generally associated with regional ST segment elevation and angina. The first description of coronary artery spasm was likely made by Heberden in 1802 when he described angina as spasmodic, occurring at rest and related to emotional factors. 1) For over 100 years, this presumed vasoconstrictor phenomenon was implicated in myocardial infarction and angina pectoris. It was not until the mid -twentieth century that the correlation between atherosclerotic plaques and angina pectoris was realized. 2) This observation lessened the interest in vasospasms as an etiology of angina, particularly because later investigations failed to observe spasms very often in patients with angina pectoris. 3) In the latter third of the twentieth century, the demonstration of coronary vasospasm during angina (Prinzmetal's angina) and as a precursor to myocardial infarction 4) resurrected interest in the vasomotor etiology of angina pectoris. 5) In recent years, our understanding of the endothelial modulation of coronary tone has evolved, and substantial insight has been provided from a number of studies over the past three decades. However, the mechanism of coronary vasospasm remains elusive.Some investigations have reported that endothelial dysfunction is present at the site of a coronary vasospasm. 6,7) However, several lines of evidence indicate that coro...