Cases reported "Angina Pectoris, Variant"

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1/26. Prinzmetal's variant angina: three case reports and a review of the literature.

    Prinzmetal's variant angina is a rare entity. When angina-like symptoms occur at rest, mostly at a specific hour in the early morning, together with transient ST segment elevations and angiographically normal arteries, provocative tests with ergonovine or acetylcholine should be performed. Endothelial dysfunction, a strong thrombotic tendency, an increased platelet aggregation together with changes in autonomic tone can trigger coronary vasospasms. Once treated with calcium antagonists and nitrates the prognosis is excellent and severe complications such as arrhythmias, myocardial infarction or sudden death are extremely rare. Coronary stenting can be useful for refractory coronary spasm, CABG can be used for important coronary atherosclerosis. This review is illustrated with three typical presentations of variant angina: a myocardial infarction without significant organic coronary atherosclerosis, an ergonovine-induced coronary spasm with a non-significant coronary lesion and a multivessel spasm complicated by ventricular arrhythmia. All these three patients became asymptomatic after a treatment with calcium antagonists and nitrates.
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2/26. Beware of the heart: the multiple picture of cardiac involvement in myositis.

    A 42-yr-old woman with dermatomyositis had two myocardial infarctions, episodes of acute chest pain and an acute lung oedema. These events were initially misinterpreted as atherosclerotic ischaemic heart disease accompanying the autoimmune disease. The lack of improvement of cardiac symptoms with anti-ischaemic and immunosuppressive drugs indicated other mechanisms. Intracoronary drug provocation as well as myocardial biopsy revealed a coincidence of small-vessel disease and vasospastic angina as a cause for the severe cardiac symptoms. After initiating therapy with high doses of calcium channel blockers, marked improvement of cardiac symptoms occurred. In the pathogenesis of cardiac involvement in dermatomyositis, two different mechanisms should be considered: inflammatory processes due to dermatomyositis and vasoconstriction caused by an impaired regulation of vascular tone, such as abnormal vessel reactivity or disturbed neuropeptide release. Signs of this generalized vasopathy are Raynaud's phenomenon, Prinzmetal's angina and small-vessel disease, which can coincide. In patients with severe cardiac symptoms and autoimmune diseases, Prinzmetal's angina should be excluded by intracoronary drug provocation using acetylcholine.
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3/26. Exercise-triggered transient R-wave enhancement and ST-segment elevation in II, III, and aVF ECG leads: a testament to the "plasticity" of the QRS complex during ischemia.

    We describe a patient with coronary artery disease who showed transiently augmented R-waves in his electrocardiogram (ECG) during the course of an exercise treadmill test (ETT), an ECG pattern occasionally associated with the hyperacute phase of myocardial infarction and variant angina. This change in the R-waves was noted in II, III, and aVF ECG leads and was associated with ST-segment elevation; both changed gradually and were normalized during the recovery period. Cardiac enzymes after ETT were negative, and arteriography revealed 3-vessel coronary artery disease, with a completely occluded right coronary artery. The ventriculogram showed very mild hypokinesis of the inferior left ventricular wall, while the global ejection fraction was 75%. These ECG changes, noted previously during ETT in precordial ECG leads, are herein reported to occur also in II, III, and aVF ECG leads. The generation of these ECG changes, which hinges upon a late unopposed depolarization occurring in the course and at the site of severe ischemic injury, constitutes a transient focal ventricular conduction abnormality.
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4/26. Prinzmetal's angina.

    Prinzmetal's angina, often referred to as "variant" angina, is a temporary increase in coronary vascular tone (vasospasm) causing a marked, but transient reduction in luminal diameter. This coronary vasospastic state is usually focal at a single site and can occur in either a normal or diseased vessel. patients are predominantly younger women who may not have the classical cardiovascular risk factors (except for cigarette use). PVA has been associated with vasospastic disorders such as Raynaud's phenomenon and migraine headaches. Arrhythmias are common and may be life threatening especially when the effects of vasospasm are seen in those ECG leads that reflect the potential variations of the epicardial surface of the left ventricle. Endothelial dysfunction has been considered as primarily responsible for PVA. The diagnosis is made by observing transient ST-segment elevation during the attack of angina. Since PVA is not a "demand"- induced symptom, but rather a supply (vasospastic) abnormality, exercise treadmill stress testing is of no value in the diagnosis of PVA. The most sensitive and specific test for PVA is the administration of ergonovine intravenously. Fifty micrograms at 5-minute intervals is given until a positive result or a maximum dose of 400 microg has been administered. When positive, the symptoms and associated ST-segment elevation should be present. nitroglycerin rapidly reverses the effects of ergonovine if refractory spasm occurs. Medical therapy classically employs vasodilator drugs, which include nitrates and calcium channel blockers. The prognosis is good when there is no significant coronary artery stenosis. Treatment of associated coronary atherosclerosis in elderly patients with PVA is advised. When PVA is associated with coronary atherosclerosis, the prognosis is determined by the severity of the underlying disease. beta-Blockers and large doses of aspirin are contraindicated in PVA.
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5/26. Multivessel variant angina unresponsive to urapidil.

    We present a case of variant angina complicated by recurrent sudden cardiac death. During coronary angiography a diffuse 3-vessel vasoconstriction was observed progressing to a more severe vasoconstriction in the mid LAD. Intracoronary administration of urapidil did not reverse the vasoconstriction of the LAD; instead an occlusive vasospasm occurred accompanied by marked ischaemia.
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6/26. "Torsade de pointes" in a patient with variant angina.

    Ventricular tachyarrhythmias have been well documented in patients with variant angina. Episodes of torsade de pointes have been described infrequently. We report a case of a 60-year-old male with a previous history of one vessel artery disease and a successful coronary angioplasty with stenting of the left anterior descending artery, who experienced an episode of angina at rest and electrocardiographic evidence of self-terminating torsade de pointes. After a negative coronary angiography and a positive hyperventilation test, the diagnosis of variant angina was considered and beta-blockers discontinued and calcium channel antagonists prescribed. No other episodes of angina were documented during the following 6 months of follow-up.
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7/26. Various 12-lead electrocardiographic findings of diffuse three-vessel coronary artery spasm.

    Electrocardiographic signs of diffuse three-vessel coronary artery spasm may show various findings including no ST segment changes, according to whether or not a difference of an electrical gradient develops between the anterior and inferior regions because of global ischemia. This study suggests that diffuse three-vessel coronary artery spasm must be considered when the 12-lead electrocardiogram (ECG) shows no important ST segment changes with episodes of angina and diffuse coronary artery spasm during an ergonovine provocation test in patients with strongly suspected variant angina.
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8/26. Angiographic demonstration of spontaneous diffuse three vessel coronary artery spasm.

    The spontaneous occurrence of diffuse three vessel coronary artery spasm was documented during routine coronary angiography in three patients with a history of variant angina. Quantitative angiographic analysis of 18 arterial segments demonstrated that the mean luminal diameter of 1.47 mm during spasm increased to 2.47 mm after the administration of nitroglycerin (p less than 0.0001). The underlying coronary arteries were normal or near normal. Although multivessel spasm has previously been considered to be uncommon and its spontaneous occurrence during angiography only rarely documented, these cases suggest that it may be more common than previously recognized. In addition to important diagnostic considerations, this phenomenon may have important implications regarding the pathophysiologic role of endothelium in coronary artery spasm.
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9/26. Biphasic response of coronary arterial diameter to intracoronary ergonovine.

    This report presents a case of paradoxical coronary arterial dilation induced by intracoronary ergonovine. When compared with the control angiogram, the right coronary artery obviously dilated with selective, intracoronary administration of cumulative doses of 5 micrograms and 15 micrograms ergonovine without concomitant hemodynamic changes. Additional intracoronary infusion of 35 micrograms ergonovine into the right coronary artery inversely increased vascular tone of the vessel associated with a focal hyperconstriction. Such a biphasic response of arterial diameter to intracoronary ergonovine was also observed in the left coronary artery, but the degree of dilation was much smaller.
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10/26. Significance of the walk-through angina phenomenon during exercise testing.

    Out of 3,900 patients who performed an exercise test at our clinic, 3 patients demonstrated a walk-through phenomenon (WTP), defined as the occurrence of mild angina during the first stages of exercise with disappearance of chest pain at higher workloads despite a greater pressure-rate product. 2 patients had variant angina, one with normal coronary arteries and the other with single vessel disease, while the third patient had stable exertional angina and a severe coronary artery disease with occlusion of two major vessels retrogradely filled by collateral channels. Repeat exercise tests failed to reproduce constantly the WTP in the 2 patients with variant angina, while in the third patient the phenomenon was repeatedly induced by exercise testing. Thus the WTP, although rarely found during exercise testing, can be observed in two subsets of patients. In variant angina the WTP is not reproducible and is probably due to coronary spasm, spontaneously subsiding during exercise. In patients with exertional angina and severe coronary artery disease, the WTP can be repeatedly observed during exercise and is likely to be secondary to a delayed vasodilation of collateral vessels. The clinical characteristics of the patients and the response to repeat exercise tests may be useful in identifying the different pathogenetic mechanisms.
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