Principal component analysis provides a better quantitative assessment of the complexity of repolarization than other ECG measurements. When applied to ARVD patients, principal component analysis of the ST-T waves recorded from the entire chest surface revealed abnormalities not detected by conventional ECG that can be considered indexes of arrhythmia vulnerability.
on behalf of the GIROC Investigators Permanent pacemaker implantation (PPI) represents a rare complication after cardiac surgery, with no uniform agreement on timing and no information on follow-up. A multicenter retrospective study was designed to assess pacemaker dependency (PMD) and longterm mortality after cardiac surgery procedures. Between 2004 and 2016, PPI-patients from 18 centers were followed. Time-to-event data were evaluated with semiparametric regression Cox models and semiparametric Fine and Gray model for competing risk framework. Of 859 (0.90%) PPI-patients, 30% were pacemaker independent (PMI) at 6 months. PMD showed higher mortality compared with PMI (10-year survival 80.1% § 2.6% and 92.2% +2.4%, respectively, log-rank p-value < 0.001) with an unadjusted hazard ratio for death of 0.36 (95% CI 0.20 to 0.65, p< 0.001 favoring PMI) and an adjusted hazard ratio of 0.19 (95% CI 0.08 to 0.45, p< 0.001 with PMD as reference). Crude cumulative incidence function of restored PMI rhythm at follow-up at 6 months, 1 year and 12 years were 30.5% (95% CI 27.3% to 33.7%), 33.7% (95% CI 30.4% to 36.9%) and 37.2% (95% CI 33.8% to 40.6%) respectively. PMI was favored by preoperative sinus rhythm with normal conduction (SR) (HR 2.37, 95% CI 1.65 to 3.40, p< 0.001), whereas coronary artery bypass grafting and aortic valve replacement were independently associated with PMD (HR 0.63, 95% CI 0.45 to 0.88, p = 0.006 and HR 0.807, 95% CI 0.65 to 0.99, p = 0.047 respectively). Time-to-implantation was not associated with increased rate of PMI.
The effect of propranolol administration on regional coronary haemodynamics were investigated in 14 patients with stable exertional angina and isolated left anterior descending artery disease. Thermodilution was used to measure great cardiac vein flow (GCVF) and anterior regional coronary resistance (ARCR) under control conditions, at peak atrial pacing, after i.v. propranolol administration (0.1 mg kg-1) and at the peak of repeated atrial pacing. Propranolol did not change peak pacing heart rate, systolic blood pressure or double product. Peak pacing GCVF decreased slightly but non-significantly after drug administration from 84 +/- 20 to 79 +/- 24 ml min-1, while ARCR increased, but again non-significantly, from 1.36 +/- 0.44 to 1.45 +/- 0.45. Analysis of individual patient responses revealed that propranolol prolonged peak pacing time and hence peak pacing heart rate (from 126 +/- 24 to 140 +/- 23 beats min-1, P less than 0.05) in five patients. In such patients, peak pacing systolic blood pressure was lower than the pre-propranolol atrial pacing (145 +/- 35 vs 165 +/- 33, P less than 0.001) so that double product remained unchanged. Moreover, peak pacing ARCR did not change after propranolol (pre-propranolol 1.47 +/- 0.46, after propranolol 1.40 +/- 0.56 mmHg.ml-1.min, P = ns) while it increased significantly in the nine patients who did not improve after the drug (before propranolol 1.30 +/- 0.44, after propranolol 1.48 +/- 0.41 mmHg.ml-1.min, P less than 0.02). These data suggest that the response to atrial pacing after i.v. propranolol administration is variable as some patients tolerate higher heart rates while others do not.(ABSTRACT TRUNCATED AT 250 WORDS)
To investigate the mechanism of the antianginal action of diltiazem in stress-induced myocardial ischemia, we studied 12 patients with stable exertional angina and disease of the proximal left anterior descending artery by measuring great cardiac vein flow (GVCF) and calculating anterior regional coronary resistance (ARCR) during myocardial ischemia induced by atrial pacing before and after intravenous administration of diltiazem (0.25 mg/kg in a bolus dose followed by continuous infusion of 0.005 mg/kg/min). Diltiazem increased the pacing time to angina from 6.9 ± 3.5 to 10.7 + 4 min (p < .001). At peak pacing heart rate was increased after diltiazem ( Circulation 73, No. 6, 1248-1253, 1986 DILTIAZEM is a calcium channel-blocking agent that has been shown to improve exercise tolerance in patients with exertional angina.'-' It is not known, however, whether the beneficial effects of the drug are achieved by a decrease in myocardial oxygen demand at any level of exertional stress or if they are a result of an increase in coronary flow.9 In this study we evaluated the effects of diltiazem on coronary hemodynamics in a selected group of patients with stable exerciseinduced angina and disease of the proximal left anterior descending artery. Thermodilution measurements of great cardiac vein flow (GCVF), representing the venous efflux from the territory supplied by the left anterior descending artery,"'-'2 were obtained at rest and during ischemia induced by atrial pacing performed before and after intravenous administration of diltiazem. The effects of the drug on anginal threshold were then related to coronary hemodynamics and changes in oxygen consumption of the myocardial region in which perfusion was jeopardized.
MethodsStudy patients. The study group consisted of 12 patients (1 1 men and one woman, mean age 55 + 7 years) with stable exertional angina and a positive exercise test result, defined as the development of chest pain and 1 mm or more ST segment depression in the precordial leads. Patients whose angina predominantly occurred at rest or who showed ST segment elevation suggestive of variant angina were not included in this study. No patient had clinical evidence of heart failure or had had a myocardial infarction within 6 months of the study. In no patient were pathologic Q waves observed in the precordial leads. The patients underwent coronary arteriography, which revealed significant coronary artery disease (> 50% diameter narrowing of one or more vessels) that in all cases involved the proximal portion of the left anterior descending artery. No patient had left main coronary artery disease.Procedure. All patients were studied while in the fasting state 1 to 10 days after coronary arteriography and none received premedication. Nitrates and nifedipine were suspended 12 hr before the study; four patients who were taking ,8-blockers were gradually weaned and the drug was discontinued at least 1 CIRCULATION by guest on May 9, 2018 http://circ.ahajournals.org/ Downloaded from
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