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Thallium-201(Tl) is the dominant agent employed for myocardial perfusion imaging for detection of coronary artery disease, assessment of myocardial viability and prognostication. Technetium-99m(Tc) labeled radionuclides have been used as excellent alternatives to Tl. This paper will review the usefulness and pitfall in myocardial perfusion single photon emission computed tomography(SPECT) in patients with coronary artery disease. From a practical standpoint, we should know what are clinical questions, clinical status of patients(history and exercise ability of patients, obesity) and diagnostic accuracy of each diagnostic protocol and the performance in the nuclear laboratory. Myocardial perfusion defects during stress SPECT are produced by a heterogeneity in coronary blood flow, which depends on severity of coronary stenosis and consequent abnormalities in flow reserve. Certain factors can affect sensitivity and specificity of Tl SPECT for detection of coronary artery disease. Accurate determination of myocardial viability is vitally important for clinical decision making for patients with left ventricular(LV) dysfunction who will most benefit from revascularization. Hibernated myocardium may result in profound regional LV dysfunction in absence of necrosis. The various approach such as stress-redistribution-reinjection imaging, rest-redistribution imaging and rest-redistribution 24 hours delayed imaging has been utilized to assess myocardial viability with Tl. Alternatively, quantitative assessment of 99mTc-methoxy-isobutyl isonitrile(MIBI) and tetrofosmin uptake reflect the degree of viability. At the present time one of the most important clinical applications of exercise myocardial perfusion SPECT is the assessment of prognosis for patients with suspected and documented coronary artery disease. Patients with normal stress perfusion SPECT have a low event rate and excellent prognosis. Stress perfusion imagings have been widely used to stratify patients into different risk groups in the United State.

Severe mitral regurgitation (MR) due to abnormal chordae tendineae as a primary cause is rare. This clinicopathologic study included four such cases which occurred among 6,500 consecutive autopsies on persons older than 60 years. This paper describes three of these cases. Case 1 was a 76-year-old woman with congestive heart failure, MR and atrial fibrillation. She died of acute myocardial infarction. The heart weighed 360 g. Mitral regurgitation was caused by a thick and long abnormal chorda originating from the posteromedial papillary muscle and protruding into the atrial surface of the middle scallop of the posterior mitral leaflet associated with prolapsed anterior mitral leaflet. Case 2 was an 81-year-old woman with MR and congestive heart failure. She died of acute myocardial infarction. The heart weighed 480 g. There were abnormal chordae tendineae with very few branches at the posterior commissure. Parts of both mitral leaflets on the sides of posterior commissure were also prolapsed. Case 3 was a 91-year-old man with MR and atrial fibrillation. He died of congestive heart failure. The heart weighed 530 g. Abnormal chordae tendineae with reticular structures originated from the anterolateral papillary muscle and protruded into the anterior mitral leaflet, which induced severe MR. These cases had abnormally protruding chordae tendineae, abnormal branching, and abnormal structures of the chordae tendineae, respectively. These abnormal chordae tendineae were considered to be congenital anomalies. Clinically all patients had a holosystolic murmur (Levine III-IV degrees), refractory congestive heart failure and atrial fibrillation. The etiology of the MR in these three patients was suspected to be ruptured chordae tendineae demonstrated on echocardiograms. These patients had heavy hearts (mean 457 g) with enlarged left atria and thickened mitral valves, which corresponded to the appearance of severe MR.