A case of painless myocardial injury probably caused by coronary artery spasm]

A 53-year-old male was admitted to the hospital due to electrocardiographic ST-segment elevation in V1-4 with ST-segment depression in the inferior leads, which suggested acute myocardial infarction. He had a cough and a slight fever without chest pain. Serum creatine kinase and its myocardial band were slightly elevated but creatine kinase value did not exceed twice the normal upper limit. Emergent coronary arteriography (CAG) revealed intact coronary arteries. The CAG in a chronic stage again revealed intact coronary arteries. Intracoronary administration of acetylcholine of 100 micrograms to the left coronary artery and 50 micrograms to the right coronary artery provoked diffuse spasm in the right and left coronary arteries. The electrocardiogram (ECG) during the right coronary artery spasm revealed ST-segment depression in the inferior leads with ST-segment elevation in V2 and V3, which resembled the ECG finding at the time of the patient's admission. With intracoronary isosorbide dinitrate, the spasm and ST-segment elevation were resolved. These findings strongly suggest that coronary spasm can cause myocardial injury indicated by a slight elevation of serum creatine kinase value.     

Myocardial ischemia in patients with fixed occlusive coronary artery disease secondary to vasospasm in the “normal” vessel

Seven patients with significant fixed occlusive coronary artery disease had coronary artery spasm in a “normal” vessel. All patients had one or more episodes of rest angina and six had exertional angina as well. Four sustained previous myocardial infarction. During spontaneous angina, five patients had ST-segment elevation in the inferior electrocardiographic leads. One patient had ST-segment elevation in anterior leads. During angiography, spasm was demonstrated in the right coronary artery in three patients and in the left anterior descending coronary artery in one patient. This study emphasizes the interaction of fixed and vasospastic disease and has strong implications concerning the management of patients with ischemic heart disease.     

Possible role of coronary spasm in acute myocardial infarction precipitated by hyperventilation

Acute myocardial infarction was precipitated by hyperventilation in a 65 year old man. His coronary arteriogram in the chronic phase showed almost normal coronary arteries. Injection of acetylcholine (50 micrograms) into the left coronary artery induced spasm of the circumflex artery with chest pain in association with ST-segment elevation in the inferior leads and ST-segment depression in the precordial leads. In this patient there may have been atherosclerosis of the coronary arteries with absent or dysfunctional endothelium, despite an almost normal angiographic appearance. In the absence of endothelium the response of the smooth muscle to acetylcholine is constriction.     

Possible role of coronary spasm in acute myocardial infarction precipitated by hyperventilation.

Acute myocardial infarction was precipitated by hyperventilation in a 65 year old man. His coronary arteriogram in the chronic phase showed almost normal coronary arteries. Injection of acetylcholine (50 micrograms) into the left coronary artery induced spasm of the circumflex artery with chest pain in association with ST-segment elevation in the inferior leads and ST-segment depression in the precordial leads. In this patient there may have been atherosclerosis of the coronary arteries with absent or dysfunctional endothelium, despite an almost normal angiographic appearance. In the absence of endothelium the response of the smooth muscle to acetylcholine is constriction.     

Acute myocardial infarction induced by ergotamine tartrate: possible role of coronary arterial spasm

A 45-year-old woman with almost normal coronary arteries suffered from acute inferior myocardial infarction after taking 2 tablets (2.0 mg) of ergotamine tartrate for headache. She had had attacks of variant angina and spasm of the right coronary artery had been demonstrated during the attack. After the recovery from myocardial infarction the intravenous injection of ergonovine maleate 0.05 mg induced spasm of the right coronary artery again. We conclude that acute myocardial infarction in this patient was probably caused by coronary arterial spasm induced by ergotamine tartrate.     

Marked ST-segment elevation in the precordial and inferior leads in right ventricular myocardial infarction: a case report

This is a report of right ventricular infarction complicated by inferior myocardial infarction in which marked ST-segment elevation was observed in the precordial and inferior leads. A 51-year-old man was admitted with chest pain of one-half hour duration. His admission ECG showed conspicuous ST-segment elevation in the precordial and inferior leads. The maximum magnitude of the ST-segment elevation in the precordial leads was 21 mm in lead V2 and 10 mm in lead II. Echocardiography showed akinesis of the right ventricular free wall and the posterior half of the left ventricle. Angiography revealed a 90% reduction in the diameter of the right coronary artery in its proximal portion, and a normal left coronary system. Recent reports have indicated that precordial ST-segment elevation may reflect right ventricular infarction. However, there has been no previous report of marked ST-segment elevation in the precordial and inferior leads. In right ventricular infarction, the currents of injury usually occur simultaneously in the right ventricular free wall and left ventricular inferior wall, and then are electrically opposed to each other. The diffuse and marked ST-segment elevation observed in this case is thus a rare phenomenon.     

Dobutamine-induced transmural myocardial ischemia in a patient with mild coronary lesions

A 70-year-old man was admitted for evaluation of retrosternal pain at rest. During infusion of dobutamine (25 μg/kg/min) the patient developed angina, ST-segment elevation in the inferior leads, and echocardiographic hypokinesia in the inferior-basal myocardial wall. Coronary angiography revealed insignificant (20-30%) stenosis of the right coronary artery and a normal remaining tree. This case suggests that dobutamine may induce transmural myocardial ischemia in patients with mild coronary lesions, probably by producing occlusive coronary spasm on a substrate of arterial endothelial dysfunction.     

Precordial ST-segment elevation caused by right coronary artery occlusion

Among 57 consecutive patients undergoing percutaneous transluminal coronary angioplasty (PTCA) of the right coronary artery, eight patients showed precordial ST-segment elevation in leads V1-3 during the procedure. The mechanism of this ST elevation was investigated reviewing the coronary angiographic findings. All patients had angina pectoris, but none had evidence of myocardial infarction. The balloon inflation time was limited to 60 sec, and 12 lead electrocardiograms were recorded every 15 sec. In the eight patients who had precordial ST-segment elevation, six had the anatomically dominant right coronary artery, and two had proportioned (balanced) left and right coronary arteries. Six patients, however, had functionally dominant left coronary arteries because of good collaterals supplying the right coronary artery from the left coronary artery. Thus, functionally, six had the dominant left coronary artery, one had proportioned coronary supply, and only one had the dominant right coronary artery. In all eight patients, the most proximal portion of the right coronary artery was occluded during PTCA, obstructing both the conus branches and the right ventricular branches. This often induced precordial ST-segment elevation in cases with the functionally dominant left or proportioned coronary artery. This ST-segment elevation seemed to represent right ventricular ischemia, as the inferior wall was protected from ischemia by good collaterals. However, precordial ST-segment elevation was rare in the functionally dominant right coronary artery even when the most proximal portion of the right coronary artery was occluded. This fact seemed due to masking of electrocardiographic manifestations of right ventricular ischemia by the dominant electrical forces of inferior wall ischemia.     

Lethal presentations of coronary artery spasm after an event-free period of six years following initial diagnosis

Isolated coronary artery spasm without atherosclerotic obstruction is an unusual cause of myocardial infarction (MI). A middle-aged woman presented to our institution in 2001 with acute inferior MI due to coronary artery spasm at the mid segment of the dominant left circumflex coronary artery. After being well for 6 years, she was readmitted again in 2007 with the same type of severe retrosternal chest pain. Electrocardiography (ECG) showed ST-segment elevation over the inferior leads. The chest pain resolved with sublingual nitroglycerin and emergency diagnostic coronary angiography showed normal coronary arteries. Two months later, the patient developed another episode of severe retrosternal chest pain at home, followed by cardiac arrest. An onsite ECG showed ventricular fibrillation and immediate defibrillation was carried out. She was readmitted to the hospital and recovered over the next few days. In view of the recurrent coronary artery spasm causing myocardial infarction and ventricular fibrillation, an implantable cardioverter defibrillator was implanted. The patient was well at 2-month follow up.     

Anterior ST-segment elevation with right coronary artery occlusion: a unique case of isolated right ventricular infarction

Anterior ST-segment elevation is the classic electrocardiographic feature of anterior left ventricular myocardial infarction due to occlusion of the left anterior descending artery. However, anterior ST-segment elevation has also been described in patients with right coronary artery occlusion, in whom concomitant inferior ST-segment elevation is also typically present. A case of proximal right coronary artery occlusion resulting in anterior ST-segment elevation without inferior ST-segment elevation is reported in this article. It is hypothesized that the inferior left ventricular wall was protected by left-to-right collaterals, as seen on coronary angiography, with resultant isolated right ventricular infarction upon proximal right coronary artery occlusion. In conclusion, this report presents a unique case of an isolated right ventricular infarction resulting in an electrocardiographic pattern mimicking anterior-wall left ventricular infarction.     

Coronary arterial spasm in angina at rest associated with transient ST-segment changes

In order to clarify the role of coronary arterial spasm in the pathogenesis of angina at rest, coronary arteriography was performed during spontaneous chest pain or following intravenous administration of ergonovine maleate in 40 patients with angina at rest. Coronary vasospasm was demonstrated in 23 patients with ST-segment elevation during chest pain (group I), in 7 with ST-segment depression (group II), and in 4 with both ST-segment depression and elevation (group III). Complete spastic occlusion of the proximal or of the midportion of the left anterior descending artery was always associated with ST-segment elevation in anterior leads. In contrast, transient ST-segment depression in anterior leads was associated with diffuse narrowing of the left anterior descending artery with slow progression of the contrast medium, or complete occlusion of a small branch or of the distal segment of the left anterior descending artery. ST-Segment elevation in inferior leads was associated with complete spastic occlusion or with significant spastic narrowing of the right coronary artery or of the circumflex artery. We conclude that coronary spasm can be demonstrated in a selected cohort of patients with angina at rest associated with transient ST-segment changes. In some cases the site and the severity of the spasm may produce varying degrees of ischemia, thus determining the direction of the ST-segment shift.     

Acute myocarditis triggering coronary spasm and mimicking acute myocardial infarction

A 24-year-old healthy man consulted to our center because of typical on-and-off chest-pain and an electrocardiogram showing ST-segment elevation in inferior leads. An urgent coronary angiography showed angiographically normal coronary arteries. Cardiovascular magnetic resonance imaging confirmed acute myocarditis. Although acute myocarditis triggering coronary spasm is an uncommon association, it is important to recognize it, particularly for the management for those patients presenting with ST-segment elevation and suspect myocardial infarction and angiographically normal coronary arteries. The present report highlights the role of cardiovascular magnetic resonance imaging to identify acute myocarditis as the underlying cause.     

Role of coronary artery spasm in ischemic heart disease. Therapeutic implications

The term coronary artery spasm should not be used interchangeably with the specific clinical syndrome "variant angina" since it does occur in other acute and chronic ischemic heart disease syndromes. The term coronary artery spasm should not be applied to patients with ischemic heart disease unless there is clinical, angiographic, and physiologic evidence of its presence. The diagnosis of coronary artery spasm is confirmed by angiography, i.e. change in caliber of the coronary arteries plus evidence of ischemia. Probable diagnosis is in patients who have the syndrome of variant angina, i.e. rest angina associated with ST segment elevation on the electrocardiogram. One can be highly suspicious that the spasm is at work in patients who have rest angina, especially those with unstable angina. One can be suspicious of patients who have variable effort angina or walk-through angina. Coronary artery spasm is a possibility in patients with an acute myocardial infarction or acute re-infarction and is also possible that sudden death in patients with normal coronary arteries can be related to coronary artery spasm. Coronary artery spasm is the usual cause of myocardial ischemia in patients with rest angina without effort angina. This has also commonly been documented in patients with rest and effort angina. There are isolated reports suggesting that patients with effort angina pectoris also develop coronary artery spasm. Coronary artery spasm has been documented to occur in association with acute myocardial infarction. Whether coronary artery spasm is the cause or the result of myocardial infarction has not been determined at this time. However, the recent combined use of intracoronary nitroglycerin and intracoronary streptokinase in patients with acute myocardial infarction has shown reversal of totally obstructed arteries and suggests the relationship between coronary artery disease, coronary artery spasm, and in situ coronary thrombosis. The incidence of sudden death in patients with documented coronary artery spasm is unknown. But, since complete heart block and/or ventricular tachycardia occur during episodes of coronary artery spasm, it is not unreasonable to assume that some patients have died as a result of these rhythm disturbances. The prognosis of patients with coronary artery spasm seems to depend on the presence or absence of severe coronary atherosclerosis, i.e. those with severe disease have a worse prognosis. Current therapy of patients with coronary artery spasm involves the use of nitrates and calcium antagonists.(ABSTRACT TRUNCATED AT 400 WORDS)     

Precordial ST-segment elevation in acute occlusion of the proximal right coronary artery

Isolated right ventricular myocardial infarction (RVMI) rarely occurs and accounts for only 3% of all myocardial infarction cases. In the literature, there are several reported isolated RVMI cases with precordial ST-segment elevation. We describe a 45-year-old man with marked ST-segment elevations in leads V1 through V4 accompanied by slight ST-segment elevations in the inferior leads (III, aVF) caused by acute occlusion of a nondominant small right coronary artery proximal to the conus branch causing isolated RVMI.     

Massive ST-segment elevation in precordial and inferior leads in right ventricular myocardial infarction

This report describes a case of right ventricular infarction in which massive ST-segment elevation in the precordial and inferior leads was observed. The maximum magnitude of the ST-segment elevation in the precordial leads was 21 mm in lead V2 and that in the inferior leads was 10 mm in lead II. Angiography revealed a reduction of 90% in the diameter of the right coronary artery in its proximal portion and a normal left coronary system. Recent reports have shown that precordial ST-segment elevation may reflect right ventricular infarction. However, no previously reported instance except our case has shown massive ST-segment elevation in both the precordial and inferior leads. In right ventricular infarction, the current of injury is usually simultaneously present in the right ventricular free wall and left ventricular inferior wall, electrically opposed to each other. Thus, the diffuse and massive ST-segment elevation observed in this study seems to be a rare phenomenon.     

Increasing pre-excitation (“concertina effect”) during vasospastic angina

A patient with Wolff-Parkinson-White syndrome and variant angina developed progressive ST-segment elevation in the inferior leads after hyperventilation-induced right coronary artery spasm. At the same time, increasing pre-excitation ("concertina effect") developed with gradual prolongation of the AH interval on His bundle ECG. The ECG changes promptly disappeared after sublingual nitroglycerin, with termination of the chest pain. Transient ischemia induced by coronary artery spasm can be an etiology of increasing pre-excitation.     

平板运动试验诱发ST段抬高对冠心病的诊断价值

目的探讨平板运动试验（TET）诱发ST段抬高对冠心病的诊断价值。方法回顾我院11例无心肌梗死而TET诱发ST段抬高患者,分析其TET心电图及冠状动脉造影（CAG）检查结果。结果 1例CAG未见固定狭窄。10例均有不同程度冠脉病变（其中1例为单支病变,9例为多支病变）,有8例冠状动脉狭窄程度达90%以上。ST段抬高导联与缺血相关冠状动脉有良好的对应关系。结论无心肌梗死者TET诱发的ST段抬高,提示冠脉痉挛或冠脉严重狭窄,且指示的缺血区域与病变冠脉一致。     

Electrocardiographic differentiation of occlusion of the left circumflex versus the right coronary artery as a cause of inferior acute myocardial infarction

To determine whether the admission electrocardiogram can identify left circumflex or right coronary artery occlusion as the cause of an inferior acute myocardial infarction (AMI), findings from electrocardiography and coronary angiography performed within 12 hours of each other were retrospectively assessed in 41 consecutive patients with inferior AMI. All patients had ST-segment elevation in 1 or more inferior leads (II, III or aVF). Of the 12 patients with circumflex coronary artery occlusion, 10 (83%) had ST-segment elevation in 1 or more lateral leads (aVL, V5 or V6) without ST-segment depression in lead I. Similar electrocardiographic findings were noted in only 1 of 29 patients (4%) with right coronary occlusion (p less than 0.001). ST-segment depression in precordial leads V1-V3 was equally prevalent in both groups. Thus, the presence of both ST-segment elevation in 2 or more inferior leads and ST-segment elevation in 1 or more lateral leads with an isoelectric or elevated ST segment in lead I identified circumflex coronary occlusion with a sensitivity of 83%, specificity of 96%, positive predictive accuracy of 91% and negative predictive accuracy of 93%. When these criteria were prospectively applied to an additional cohort of 19 consecutive patients with inferior AMI (5 with left circumflex and 14 with right coronary artery occlusion), presence of left circumflex coronary artery occlusion was predicted with a sensitivity of 80%, specificity of 93%, positive predictive accuracy of 100% and negative predictive accuracy of 93%. Thus, the admission 12-lead electrocardiogram can assist in differentiating left circumflex from right coronary artery occlusion in patients with inferior AMI.     

Recurrence of Prinzmetal angina seven years following aortocoronary bypass surgery: a clinical and angiographic follow-up.

A patient with Prinzmetal angina and ST segment elevation in the anterior ECG leads became asymptomatic after a 50% left anterior descending coronary artery stenosis was bypassed. However, seven years later Prinzmetal angina recurred but with ST segment elevation in the inferior ECG leads. Although the coronary bypass graft had remained patent, the proximal and distal left anterior descending coronary artery was occluded. No significant stenosis was present in the right coronary artery. Perhexiline maleate controlled his symptoms but when the drug was stopped because of side effects an acute inferior myocardial infarction occurred.     

Cold pressor test and variant angina

A transient complete coronary occlusion due to spasm was induced by the cold pressor test in a 51-year-old man with variant angina. Arteriography before the test revealed a normal left coronary artery and only minor irregularities of the mid-portion of the right coronary artery. Three minutes after cold stimulation, angina pectoris accompanied by ST-segment elevation was observed in lead II ECG. Simultaneous coronary arteriography during the attack showed a complete occlusion of the proximal right coronary artery due to spasm. The anginal attack together with spastic occlusion disappeared after administration of 0.8 mg of nitroglycerin. Thus, the cold pressor test can trigger coronary artery spasm and may even lead to a total occlusion in patients with variant angina. Individuals with variant angina may be subjected to additional risk when exposed to cold temperatures.