Clinical significance of elevated levels of cardiac troponin T in patients with chronic heart failure.

Cardiac troponin T, measured by second-generation assay, is a highly sensitive and specific marker of minor myocardial damage. Cardiac troponin T was elevated in patients with severe chronic heart failure; it identifies those with latent and progressive myocardial damage and those who are at increased risk of cardiac events.

An autopsy case of familial idiopathic dilatation of bilateral atria.

A 59-year-old male patient was followed up for congestive heart failure. Echo cardiogram showed no abnormal findings other than a remarkable dilatation of the bilateral atria. The coronary arteries and left ventricular contraction were normal. Left ventricular endomyocardial biopsy showed no significant abnormal findings. Further, we examined his siblings using dynamic magnetic resonance imaging (MRI) and found that they all also had dilated bilateral atria. After several hospitalizations, the proband died from cardiogenic shock. Pathological findings showed nonspecific change in bilateral atria and ventricles. This is a very rare case of familial idiopathic dilatation of bilateral atria.

Origin and pathophysiological role of increased plasma endothelin-1 in patients with acute myocardial infarction.

To investigate the origin and pathophysiological role of increased plasma endothelin-1 (endothelin-1) concentration in patients with acute myocardial infarction (AMI), the authors measured plasma endothelin-1 sequentially after the onset of AMI and analyzed the origin by the simultaneously obtained blood samples from the radial artery, right atrium, and pulmonary artery in 28 patients with AMI. The data were correlated with cardiovascular hemodynamics, infarct size, and coronary arteriographic findings. Arterial endothelin-1 at twenty-four and seventy-two hours significantly correlated with mean pulmonary arterial pressure (r = 0.48, r = 0.46, P < 0.05, respectively), central venous pressure (r = 0.42 and 0.51, P < 0.05, respectively), and pulmonary vascular resistance (r = 0.42, r = 0.42, P < 0.05), and endothelin-1 at one hundred twenty hour significantly correlated with peak creatine kinase (r = 0.53, P < 0.05) and creatine kinase isozyme MB (r = 0.58, P < 0.01). Simultaneous blood samples showed no significant difference in endothelin-1 concentrations among them. However, a subgroup of patients with endothelin-1 concenration higher in the radial artery than that in the right atrium showed a significantly higher mean pulmonary arterial pressure (25.2 +/- 6.5 vs 17.0 +/- 1.6 mmHg, P < 0.05), peak creatine kinase (3594 +/- 1597 vs 865 +/- 495 IU/L, P < 0.05), and peak creatine kinase MB (214 +/- 91 vs 69 +/- 22 IU/L, P < 0.05) as compared with those in patients in whom endothelin-1 was higher in the right atrium than in the radial artery. Increased plasma endothelin-1 concentration in the early stage of AMI reflects higher pulmonary artery pressure and elevated pulmonary vascular resistance, while that in the later stage is related to the infarct size. The production of endothelin-1 in patients with severe pump failure may be accerelated in the pulmonary vascular bed, left ventricle, or systemic arterial trees, and the main origin in the later stage is possibly coronary vasculature in the infarcted area.

[Evaluation of acute myocardial infarction by 201T1 single-photon emission computed tomography using scoring system].

In 36 patients with acute myocardial infarction (AMI) 201T1 single-photon emission computed tomography (SPECT) examinations were performed in a relatively early phase of AMI. The short and long axis views of the left ventricle (LV) were divided into 6 segments. Images of each segment were assigned scores (segmental scores) based on a visual evaluation of the extent of 210T1 accumulations as follows: 1 = normal; 2 = relatively low; 3 = low; 4 = severely low; 5 = cold. The sum total of the segmental scores constituted the SPECT score. SPECT scores were compared with maxGOT, maxLDH, maxCPK and maxCK-MB, Killip classification and Forrester hemodynamic subset on admission, and LV ejection fraction (LVEF). Segmental scores were compared with LV wall motion evaluated by left ventriculography. The results are summarized as follows: 1) There were significant correlations between SPECT scores and maxGOT, maxLDH, maxCPK and maxCK-MB (r = 0.62, r = 0.60, r = 0.51 and r = 0.39, respectively). 2) SPECT scores in patients with Killip group III were significantly higher than in patients with Killip group I + II (p less than 0.05). However, no significant differences in maxGOT, maxLDH, maxCPK and maxCK-MB were observed between patients with Killip group III and those with Killip group I + II. 3) SPECT scores were significantly higher in patients with Forrester group III + IV than in patients with Forrester group I + II (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

[Clinical investigation of inhomogeneity of washout rate in dipyridamole stress thallium scintigraphy: implication of new parameter for the indication of coronary intervention].

OBJECTIVES: The standard deviation of the washout rate in dipyridamole stress thallium-201 myocardial single photon emission computed tomography (SPECT) was correlated with the severity of coronary artery lesions and the viability of ischemic myocardium to provide a new quantitative parameter for judging indications for coronary intervention therapy. METHODS: Dipyridamole stress thallium-201 SPECT was performed in 233 patients for differential diagnosis of angina pectoris during the 40 months beginning in October 1995, and 57 patients were investigated who underwent coronary angiography within 6 months of the SPECT. The washout rate standard deviation (WRSD) in 720 fractions in the bull's-eye view of the SPECT was determined. The conventional washout rate extent score (WRES) and washout rate severity score (WRSS) on the washout rate map were also determined. Based on the coronary angiography findings, patients were divided into 3 groups: zero-vessel group (zero-vessel disease, n = 20), one-vessel group (one-vessel disease, n = 18), and multivessel group (two- or three-vessel disease, n = 19). The patients were also divided into 2 other groups: Int group (n = 21), who underwent coronary intervention therapy, and Med group (n = 36), in whom intervention therapy was not indicated. RESULTS: All 3 parameters, WRSD, WRES and WRSS, showed significant differences between the 3 groups, and more coronary arteries affected by coronary artery stenosis were associated with higher WRSD (zero-vessel group: 5.4 +/- 1.5, one-vessel group: 7.0 +/- 3.7, multivessel group 11.4 +/- 6.7; p < 0.001), WRES (3.3 +/- 5.0, 15.5 +/- 18.1, 23.0 +/- 25.4; p < 0.01), and WRSS (1.4 +/- 2.8, 25.4 +/- 40.2, 84.8 +/- 114.5; p < 0.01). WRSD (Med group: 5.9 +/- 2.7, Int group: 11.3 +/- 6.4; p < 0.001), WRES (7.3 +/- 12.0, 24.7 +/- 24.9; p < 0.01), and WRSS (9.9 +/- 29.3, 82.9 +/- 108.2; p < 0.01) were all significantly higher in the Int group compared with the Med group. There were significant correlations between Gensini's score and WRSD (r = 0.51, p = 0.00005), WRES (r = 0.37, p = 0.005), and WRSS (r = 0.29, p = 0.03). The cutoff values for the indications for coronary intervention therapy were established for each of the 3 parameters as the maximum value of average sensitivity and specificity as follows: WRSD > 9.0 (sensitivity 0.62, specificity 0.89, positive predictive value 0.76, negative predictive value 0.24); WRES > 10.0 (0.62, 0.69, 0.54, 0.46, respectively); WRSS > 13.0 (0.62, 0.83, 0.68, 0.32, respectively). WRSD > 9.0 had the highest specificity and positive predictive value for judging indications. CONCLUSIONS: A new quantitative parameter, WRSD > 9.0, suggests the presence of viable and curable ischemic myocardium as an indication for coronary intervention therapy.

Pathophysiological analysis of serum troponin T release kinetics in evolving ischemic myocardial injury.

The present study measured cardiac troponin T(TnT) for the pathophysiological analysis of evolving ischemic myocardial injury in 35 patients with unstable angina (3: Class IB, 32: Class IIIB) and in 40 patients undergoing coronary reperfusion therapy for acute myocardial infarction. Serum TnT, creatine kinase (CK), CKMB, myoglobin (Mb), and myosin light chain 1 (MLC1) were measured every 2-24 h for 10 days after admission to the CCU. In patients with unstable angina, positive test results were detected in 65.7% for TnT, 20% for CK, 37.1% for CKMB, 60.9% for Mb, and 26% for MLC1. Of the 23 patients with positive TnT, 12 (52.2%) had cardiac events. Of the 12 patients with negative TnT, 11 (91.6%) were event-free. All of the patients who developed cardiac events showed a persistent (n = 10) or delayed elevation (n = 2) pattern 28-120 h beforehand. The sensitivity for predicting cardiac events was 92.3% for TnT, 80% for Mb, 53.8% for CKMB, and 50% for MLC1. In patients with acute myocardial infarction, TnT release kinetics showed 2 peaks after coronary reperfusion therapy. TnT values at the 1st peak significantly correlated with maximum CKMB (r = 0.70, p < 0.05) and early-stage left ventricular wall motion score (r = 0.60, p < 0.05), while 2nd-peak TnT values significantly correlated with maximum MLC1 (r = 0.59, p < 0.05), the T1-SPECT score (r = 0.78, p < 0.05) and left ventricular ejection fraction (r = -0.74, p < 0.05) in the convalescent stage. The 2nd/1st-peak TnT ratio significantly correlated with the nQ/nST elevation index (ratio of the number of leads developing abnormal Q-wave 1 week after the onset to the number of leads showing ST elevation of more than 1 mm at admission) (r = 0.63, p < 0.05) in patients with anterior myocardial infarction. These data indicate that persistent release of TnT reflects progressive irreversible myocardial damage in unstable angina and indicates a risk of future cardiac events. In acute myocardial infarction, the 2nd/1st-peak TnT ratio in patients undergoing coronary reperfusion therapy may be useful for the quantitative evaluation of myocardial salvage.