Decreased soluble cell adhesion molecules after tirofiban infusion in patients with unstable angina pectoris

AIM: The inflammatory response, initiated by neutrophil and monocyte adhesion to endothelial cells, is important in the pathogenesis of acute coronary syndromes. Platelets play an important role in inflammatory process by interacting with monocytes and neutrophils. In this study, we investigated the effect of tirofiban on the levels of cell adhesion molecules (soluble intercellular adhesion molecule-1, sICAM-1, and vascular cell adhesion molecule-1, sVCAM-1) in patients with unstable angina pectoris (AP). METHODS: Thirty-five patients with unstable AP (Group I), ten patients with stable AP (Group II) and ten subjects who had angiographycally normal coronary arteries (Group III) were included the study. Group I was divided into two subgroups for the specific treatment regimens: Group IA (n = 15) received tirofiban and Group IB (n = 20) did not. Blood samples for investigating the cell adhesion molecules were drawn at zero time (baseline; 0 h) in all patients and at 72 h in Group I. RESULTS: The baseline levels of sICAM-1 and sVCAM-1 were higher in Group I than in Groups II and III. They were higher in Group IA than in Group IB. However, the sICAM-1 and sVCAM-1 levels decreased significantly in Group IA after tirofiban infusion. In contrast, these levels remained unchanged or were increased above the baseline value in Group IB at 72 h. CONCLUSION: The levels of cell adhesion molecules in patients with unstable AP decreased significantly after tirofiban infusion. Inhibition of platelet function by specific glycoprotein IIb/IIIa antagonists may decrease platelet-mediated inflammation and the ischemic end-point

Inferior ST-segment elevation due to metastatic cardiac tumor

There are numerous causes for ST-segment elevation on ECG, the tumoral invasion of the heart being a rarer one. Because the management will differ one should always keep in mind the presence of such entity. Here we report a case of persistent ST-segment elevation due to a metastatic cardiac tumor. (C) 2022 Elsevier Inc. All rights reserved

Is a drug-challenge test with propafenone adequate to exclude Brugada syndrome?

WOS: 000318862900016PubMed ID: 23613002Brugada syndrome is associated with sudden cardiac death in patients with a structurally normal heart. The electrocardiogram (ECG) pattern of Brugada syndrome is characterised by complete or incomplete right bundle branch block and ST-segment elevation in the right precordial leads. These ECG signs may not always be apparent but can be unmasked with certain anti-arrhythmia agents. We report here a case of a 26-year-old woman without detectable structural heart disease but with a history of syncope, cardiac arrest, intubation and defibrillation for ventricular fibrillation. We performed challenge tests with propafenone and ajmaline. After infusion of propafenone, there were minimal ECG changes which were not diagnostic for Brugada syndrome. One week later the provocation test was repeated with ajmaline. During infusion of ajmaline, prominent J waves and ST-segment elevation appeared in the right precordial leads (V1-3). Premature ventricular complexes were seen on a 12-lead ECG. The patient's ECG showed Brugada type I pattern. She received an internal cardioverter/defibrillator and was discharged with a beta-blocker

Primary cardiac amyloidosis mimicking interstitial lung disease and bleeding diathesis: A case report

WOS: 000249123500002PubMed ID: 17389204Primary amyloidosis is a rare systemic disease due to various organ involvements that can lead to atypical clinical findings. In this article, we discuss a case of primary cardiac amyloidosis in a patient presenting with bleeding eyelids and interstitial lung disease

Primary Cardiac Amyloidosis Mimicking Interstitial Lung Disease and Bleeding Diathesis: A Case Report

WOS: 000249123500002PubMed ID: 17389204Primary amyloidosis is a rare systemic disease due to various organ involvements that can lead to atypical clinical findings. In this article, we discuss a case of primary cardiac amyloidosis in a patient presenting with bleeding eyelids and interstitial lung disease

Myocardial bridge: a bridge to atherosclerosis

WOS: 000253867900004PubMed ID: 17347068Objective: Myocardial bridge (MB) is a congenital anomaly characterized by narrowing during systole of some of the epicardial coronary arterial segments running in the myocardium. Although, it is considered as a benign anomaly, it may lead to such complications as acute myocardial infarction, ventricular tachycardia, syncope, atrioventricular block and sudden cardiac death. In this study, we aimed to investigate demographic, clinical and angiographic characteristics of the patients with MB found on coronary angiography. Methods: The present study included 71 patients with MB found on coronary angiographies performed in our institution between January 1999 and September 2003. Based on the findings on angiography, the patients were subdivided into group A (n=41) and group B (n=30). The patients in the group A had no atherosclerotic lesion and the patients in the group B had coronary artery disease in addition to MB. Angiographic, demographic and clinical characteristics of both groups were compared. Results: There were no differences between two groups in distribution of gender and risk factors of coronary artery diseases whereas mean age of the patients in the group A was lower (47 +/- 5 years vs 55 +/- 11 years, p = 0.01). Frequency of two or more risk factors for coronary artery disease in a particular patient was significantly higher in the group B (55% vs 30%, p = 0.03). Myocardial bridge was located at proximal or mid segments of left anterior descending artery (LAD) in 40 patients whereas its presence in both LAD and right coronary artery was found only in one patient in group A. Mean bridging percent was 43 +/- 27% in group A. Localization of MB was LAD in 29 patients of group B, which was significantly higher than in group A (p<0.05). Atherosclerotic narrowing developed in only LAD in 14 patients, LAD and other vessels in 7 patients and in the vessels without MB in 9 patients. In patients with MB in LAD atherosclerotic narrowing of vessel developed proximally to the MB. Clinically, stable angina pactoris was seen more frequently in group A than group B (70% vs 35%, p = 0.01), whereas the frequency of acute coronary syndrome was higher in group B (65% vs 30%, p=0.04). In regard to therapeutic approach, more patients in the group A received medical management (80% vs 50%, p=0.01), while more patients in the group B underwent surgical and percutaneous interventions (50% vs 18%, p=0.04). Conclusion: Myocardial bridge probability should be considered in young patients presenting with angina or if the same symptoms are persistent in the patients without more than one risk factor for coronary artery disease. Myocardial bridge may initiate the development of atherosclerotic lesion or may facilitate progression of atherosclerosis in the proximal segment of the vessel. The risk of acute coronary syndrome rises when atherosclerosis is superimposed on MB. Myocardial bridge should be considered in the young patients, presenting with angina or its equivalents without atherosclerotic lesions on coronary angiography