Prolactin and leptin are newly recognized platelet co-stimulators due to enhancement of ADP-induced platelet aggregation. The aim of our study was to assess whether both hormones prolactin and leptin play a role as co-activators of platelet activation in patients with acute coronary syndromes. Twenty-one patients with acute coronary syndromes, 10 with stable angina pectoris and 10 controls were studied. Patients with acute coronary syndromes showed significantly higher prolactin and leptin values and a significant increased P-selectin expression on platelets compared to patients with stable angina pectoris or controls. However, patients with acute myocardial infarction as a subgroup of acute coronary syndromes showed the highest prolactin levels as well as ADP stimulated P-selectin expression. In the myocardial infarction subgroup prolactin values showed a significant correlation to ADP stimulated P-selectin expression on platelets (r (2)=0.41; p=0.025), whereas leptin was not correlated. Our data indicate an association between increased prolactin values and enhanced P-selectin expression on platelets in patients with acute coronary syndromes. Therefore, the stress hormone prolactin could be a co-stimulator of platelet activation in these patients. In contrast, the putative platelet activator leptin does not seem to play a major role in acute coronary syndromes.

No abstract

The effect of beta-adrenergic antagonists on ET-1 production of the endothelium may at least partially explain the efficacy of beta-blockers in the treatment of diseases such as advanced heart failure, essential hypertension as well as acute coronary syndromes.

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Interobserver variability for the quantification of non-calcified plaque volumes in 64-slice MDCT is substantial. Interobserver variability in the LAD was significantly lower than in the LCX and the RCA. This might be due to a larger mean plaque volume and better image quality in the LAD than in other coronary arteries.

No abstract

The prognostic significance of a preoperative echocardiographic left ventricular endsystolic dimension (ESD) greater than 55 mm and/or fractional shortening (FS) of 25% or less was evaluated retrospectively in 84 patients who had undergone aortic valve replacement for isolated chronic aortic regurgitation due to various causes. Postoperative survival, improvement in symptoms, and echocardiographic evidence of regression of left ventricular dilatation and hypertrophy were compared between patients with a preoperative ESD greater than 55 mm (category 1) and those with an ESD of 55 mm or less (category 2) and between patients with FS of 25% or less (category 3) and those with FS greater than 25% (category 4). Patients in categories 1 and 3 had a higher preoperative left ventricular end-diastolic dimension (EDD) and cross-sectional area than those in categories 2 and 4, respectively, but their preoperative functional impairment (NYHA class) was similar. There were 13 deaths, only two of which (one early, one late) could be attributed to left ventricular dysfunction. In both, FS was 25% or less and in one ESD was greater than 55 mm. There was a weak association without useful positive predictive value between the echocardiographic variables and postoperative death due to all causes. Among 42 patients with a preoperative ESD greater than 55 mm and/or FS of 25% or less, 33 (79%) were alive at a mean follow-up of 29.5 months. Symptoms improved in all categories of survivors, with the postoperative NYHA class being similar between categories 1 and 2 and between categories 3 and 4. Among 48 survivors with high-quality echocardiograms both before and after surgery, EDD fell in all groups but fell to a lesser extent in category 3 than in category 4. Postoperative cross-sectional area fell to the same level in all categories. Follow-up intervals were similar in all categories. We conclude that in patients undergoing aortic valve replacement for chronic aortic regurgitation, a preoperative ESD greater than 55 mm or an FS of 25% or less does not reliably predict early or late death, does not correlate with lack of improvement in symptoms, and does not preclude postoperative regression of left ventricular dilatation and hypertrophy. Thus these echocardiographic criteria alone cannot be used for the timing of surgical intervention in these patients. Circulation 71, No. 4, 669-680, 1985

In 74 mongrel dogs 0.02 ml air/kg of body weight was injected into the left anterior descending coronary artery (LAD). Forty-three dogs were studied without (group I) and 31 with (group II) extracorporeal circulation (ECC). Time course and extent of myocardial ischemia were assessed by continous thermographic measurements as well as by fluorescence techniques. Coronary air embolism resulted in an immediate decrease of myocardial temperature associated with transmural ischemia. In 31 surviving dogs (72%) of group I this phenomenon was fully reversible within 8.7 minutes as compared with 5.4 minutes in 100% of the surviving dogs from group II. No postembolic death occurred in the group II animals. In group II the postembolic temperature decrease was significantly less than that in group I, and, in addition, the myocardial area involved was significantly smaller. The results indicate that the extent of myocardial ischemia following coronary air embolism and its time course can be well-documented by means of thermocardiography; using extracorporeal circulation survival can be improved and myocardial damage minimized.