The value of 24-hour images after rest thallium injection.

Rest (201) Tl imaging has been used for detecting viability, but the ideal timing for imaging after injection to maximally estimate viability is not well established. Thirty patients with fixed or incompletely reversible defects on 4 h redistribution SPECT imaging after thallium rest injection underwent 24 h imaging. Global redistribution was subjectively rated none, minimal or meaningful by two experienced observers. Fourteen patients had no meaningful redistribution at either 4 h or 24 h. Ten patients had meaningful redistribution at 4 h only. Six patients had no meaningful redistribution at 4 h but did at 24 h. Defect size was quantified using a 70% threshold. For the total group, defect size was smaller at 4 h compared to immediate imaging (38+/-18% vs 41+/-19%, P=0.06) and smaller still at 24 h (36+/-16% vs 38+/-18%, P=0.02). Later (24 h) redistribution images detected additional redistribution in 30% of the patients who did not have meaningful redistribution on early (4 h) images, and in 8% of the segments which were abnormal at 4 h. It is concluded that, in patients who have incompletely reversible defects on early redistribution imaging at 4 h, late redistribution imaging after 24 h will demonstrate additional redistribution in 30% of the patients.

Prognostic value of vasodilator myocardial perfusion imaging in patients with left bundle-branch block.

BACKGROUND: The prognostic value of tomographic myocardial perfusion imaging with dipyridamole or adenosine in patients with left bundle-branch block has not been established. METHODS AND RESULTS: The study group consisted of 245 patients with left bundle-branch block who underwent tomographic (single photon emission tomography) myocardial perfusion imaging with thallium-201 (n=173) or technetium-99m sestamibi (n=72) and either dipyridamole (n=153) or adenosine (n=92) stress. Patients were prospectively classified into two groups. Patients were classified as "high risk" if they had (1) a large severe fixed defect (n=28), (2) a large reversible defect (n=36), or (3) cardiac enlargement and either increased pulmonary uptake (thallium) or a decreased resting ejection fraction (sestamibi) (n=20). The remaining 161 patients (66% of the study group) were at "low risk." Follow-up was 99% complete at 3+/-1.4 years. Three-year overall survival was 57% in the high-risk group compared with 87% in the low-risk group (P<.0001). Survival free of cardiac death/nonfatal myocardial infarction/cardiac transplantation was 55% in the high-risk group and 93% in the low-risk group (P<.0001). The presence of a high-risk scan had significant incremental prognostic value after adjustment for age, sex, diabetes, and previous myocardial infarction (P<.0001). Patients with a low-risk scan had an overall survival that was not significantly different from that of a US age-matched population (P=.86). CONCLUSIONS: Tomographic myocardial perfusion imaging with adenosine or dipyridamole stress provides important prognostic information in patients with left bundle-branch block, which is incremental to clinical assessment.

Mechanical strain increases smooth muscle and decreases nonmuscle myosin expression in rat vascular smooth muscle cells.

The effect of cyclic (1-Hz) mechanical strain on expression of myosin heavy chain isoforms was examined in neonatal rat vascular smooth muscle cells cultured on silicone elastomer plates. Myosin heavy chain isoforms were identified by immunoblot using antibodies recognizing (1) smooth muscle myosin heavy chain isoforms SM-1 and SM-2, (2) SM-1 exclusively, and (3) nonmuscle myosin heavy chains A and B. In response to 36 to 72 hours of strain, SM-1 and SM-2 increased by fourfold to sixfold, whereas nonmuscle myosin A decreased to 30% of control. Nonmuscle myosin B was unaffected by strain. SM-1 mRNA increased by twofold to threefold after 12 hours of strain but decreased toward control levels thereafter. SM-2 mRNA was only barely detectable. Nonmuscle myosin A mRNA decreased to 50% of control after 3 hours of strain and then returned to the control level. Since these cells secrete platelet-derived growth factor (PDGF) in response to strain, we assessed the effects of PDGF on myosin isoform expression. Exogenous PDGF (10 ng/mL) decreased SM-1 expression by 35% and increased nonmuscle myosin expression twofold, opposite the effect of strain. In cells exposed to strain with neutralizing antibodies to PDGF-AB, the strain-induced increase in SM-1 was enhanced 10-fold, and nonmuscle myosin A was reduced to 40% of control. Finally, the effect of extracellular matrix on transduction of the strain signal was studied. Forty-eight hours of cyclic strain increased SM-1 by twofold in cells cultured on collagen type 1 and threefold in cells cultured on laminin. In fibronectin-cultured cells, strain elicited no increase in SM-1. Thus, mechanical strain, sensed through specific interactions with the matrix, can alter myosin isoform expression toward that found in a more differentiated state.

Determinants of infarct size in acute myocardial infarction in patients treated with reperfusion therapy.

Infarct size after reperfusion therapy is determined by the extent of myocardium at risk, the degree of residual blood flow within the jeopardized zone, and the duration of coronary occlusion. This review article will explore the noninvasive methods that have been used to measure these variables. Recent advances in nuclear cardiology techniques will be discussed in detail, because new agents have the ability to accurately quantify these variables.