technetium-tc-99m-pyrophosphate and Coronary-Vasospasm

Because of recent findings, a reassessment is needed of the concept that rest angina associated with ST-segment depression is due to a spontaneous, transient increase of blood pressure or heart rate, or both, in the presence of critical coronary artery stenosis. Continuous hemodynamic and electrocardiographic recordings done before and during attacks of rest angina and thallium-201 scintigrams done during pain indicate that a transient reduction of flow is the immediate cause of ischemia in most, but not all, instances. Flow reduction, in turn, appears to be due to coronary arterial spasm or platelet aggregation, or both, acting at a site of atherosclerotic narrowing. Therapy for unstable rest angina should include measures to prevent both transient reductions of flow and increases of myocardial oxygen consumption. A combination of long-acting nitrates, a beta-blocker, a calcium-channel blocker, and aspirin or heparin is suggested for this purpose. Intravenous nitroglycerin is useful when angina occurs despite this therapy or when frequent attacks of ischemia are occurring at the time of admission.

Topics: Angina Pectoris; Angina, Unstable; Coronary Angiography; Coronary Disease; Coronary Vasospasm; Diphosphates; Electrocardiography; Hemodynamics; Humans; Krypton; Myocardium; Platelet Aggregation; Radioisotopes; Rest; Rubidium; Technetium; Technetium Tc 99m Pyrophosphate; Thallium

A 55-yr-old man underwent surgery. Soon after the procedure was finished, the patient complained of chest pain, and the electrocardiogram showed increase in the ST-segment in some leads. Emergency angiography showed normal coronary arteries, but there was asynergy in the left ventricle, and delayed filling of contrast medium was observed in the LCA. An intracoronary infusion of isosorbide dinitrate did not improve the delayed filling of contrast medium or ST segment increase in the electrocardiogram. Soon after nicorandil was injected into the LCA, the patient's symptoms, electrocardiogram, and delayed filling of contrast medium dramatically improved. On the second day, initial imaging by 123I-BMIPP myocardial SPECT showed a moderate increase in tracer uptake in the apico-anteroseptal region and a moderate decrease in tracer uptake in the lateral region, in which the first left ventriculography showed akinesis, and delayed imaging revealed a moderate increase in tracer uptake in the apical region and a high washout of 123I-BMIPP in the anteroseptal and lateral regions. On the sixth day, initial imaging by 123I-BMIPP myocardial SPECT showed a moderate decrease in tracer uptake in the apical and lateral regions and a mild decrease in tracer uptake in the anteroseptal region, and delayed imaging revealed a moderate increase in tracer uptake in the apical region and a high washout of 123I-BMIPP in the anteroseptal and lateral regions. By the 30th day, 123I-BMIPP myocardial SPECT had normalized. We consider that these dynamic changes in 123I-BMIPP myocardial SPECT imaging may reflect metabolic changes in fatty acids in the ischemic state, the size of the triacylglycerol pool, and the degree of turnover in the triacylglycerol pool.

Topics: Coronary Vasospasm; Electrocardiography; Fatty Acids; Humans; Iodine Radioisotopes; Iodobenzenes; Male; Middle Aged; Myocardial Stunning; Organophosphorus Compounds; Organotechnetium Compounds; Technetium Tc 99m Pyrophosphate; Tomography, Emission-Computed, Single-Photon; Triglycerides

Among 144 patients with hypertrophic cardiomyopathy, eight (58.3 +/- 7.0 years, M:F = 7:1) had complicating myocardial infarction, which was diagnosed clinically and by elevated cardiac enzymes or new Q-waves on electrocardiography. Coronary occlusion or stenosis evidenced by coronary angiography and nuclear cardiological findings were investigated. In six of the eight patients, coronary atherosclerosis caused infarction. These patients had many coronary risk factors compared to the other two patients. Sixteen of the 144 patients (11%) with hypertrophic cardiomyopathy had coronary atherosclerosis, the rate of which is reportedly 10 to 20%. Two of the eight patients had no coronary atherosclerosis. One patient had a diffusely spastic diathesis provoked by the intravenous administration of ergonovine maleate during coronary angiography, suggesting that coronary spasm caused myocardial infarction. The other patient had recurrent episodes of supraventricular tachyarrhythmia and no evidence of spasm during coronary angiography, suggesting coronary embolism as a cause of myocardial infarction. Myocardial infarction in patients with hypertrophic cardiomyopathy and normal coronary arteries as advocated by Maron et al. may have such pathogenesis. We conclude that coronary angiography may be mandatory in patients with hypertrophic cardiomyopathy, especially those who have many coronary risk factors and anginal symptoms. In these patients, ST-T changes and abnormal Q-waves on electrocardiography sometimes may be misleading when diagnosing the occurrence of acute myocardial infarction by electrocardiography alone. In such cases, infarct-avid scintigraphy with 99 m-Tc pyrophosphate is preferable.

Topics: Adult; Aged; Cardiomyopathy, Hypertrophic; Coronary Angiography; Coronary Artery Disease; Coronary Vasospasm; Diphosphates; Electrocardiography; Embolism; Female; Heart; Heart Ventricles; Humans; Male; Middle Aged; Myocardial Infarction; Radionuclide Imaging; Technetium; Technetium Tc 99m Pyrophosphate; Thallium Radioisotopes