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Biomedical subjects

Y Birnbaum

Publications and source records attributed to Y Birnbaum.

121 records · Page 7Linked to original sources
PubMed1992

An unusual cause of recurrent angina two years after coronary artery bypass grafting: fistula between internal mammary artery graft to pulmonary vasculature.

A 55-year-old man developed recurrent angina pectoris 2 years after coronary artery bypass grafting. Cardiac catheterization demonstrated that the venous grafts were patent, but selective left internal mammary angiogram showed multiple fistulous connections between the internal mammary artery and the pulmonary vasculature of the left upper lobe. After surgical correction of the fistula, the angina resolved. Only three previous cases of acquired internal mammary artery graft fistulas draining to the pulmonary vasculature have been described. The etiology, clinical presentation, and management of an internal mammary artery fistula to the pulmonary vasculature are discussed.

Angina Pectoris↗
PubMed1992

Electrocardiographic Q-waves inconstancy during thrombolysis in acute anterior wall myocardial infarction.

It is the purpose of this paper to describe the electrocardiographic inconstancy of Q-waves during administration of thrombolytic therapy. This was documented in four patients given streptokinase early in the course of anterior wall myocardial infarction. Understanding the pathogenesis of sequential dynamic variations of Q-waves in this setting may offer important insights into coronary physiology and management of acute coronary events. We discuss the possible explanations for such changes with respect to tissue viability, dynamic vascular changes and electrophysiological properties of the reperfused infarcted myocardium.

Angioplasty, Balloon, Coronary↗
PubMed1989

[Cardiac involvement in inflammatory bowel disease].

A 67-year-old man with ulcerative colitis of 1 year's duration was hospitalized with myopericarditis. Clinical manifestations were pleuritic pain, palpitation and fever. There was atrial fibrillation and supraventricular tachycardia with ST elevation in all leads. He recovered under treatment with indomethacin. No etiology other than the bowel disease was found. According to the literature, heart involvement in inflammatory bowel disease is rare; it is seen more frequently in men and in those with ulcerative colitis. This complication is not related to the activity of the bowel disease. The heart involvement responds well to either nonsteroidal anti-inflammatory drugs or to corticosteroids.

Aged↗
PubMedDate not supplied

Is preconditioning by nicotine responsible for the better prognosis in smokers with acute myocardial infarction?

Cigarette smoking is a well-known risk factor for acute myocardial infarction and sudden death. However, a history of smoking consistently has been associated with better hospital outcome in patients with acute myocardial infarction. The mechanism for the better outcome in smokers is not clear. It has been suggested that nicotine may have a "preconditioning-like" effect. This study assesses whether nicotine attenuates myocardial infarct size. Anesthetized rabbits were randomized to receive infusion of nicotine 80 micrograms/kg (n = 13), or saline (n = 12) over 10 min. Twenty minutes after termination of infusion all rabbits underwent 30 min of coronary artery occlusion and 4 h of reperfusion. Risk zone was assessed by blue dye and infarct size by tetrazolium staining. Nicotine did not affect regional myocardial blood flow 15 min after treatment, during occlusion or during reperfusion. Heart rate and mean systemic blood pressure were similar between the groups. Nicotine serum levels during occlusion were 9.5-22.0 ng/ml in the treated group, which are comparable to levels found in human smokers. No differences were found in the risk zone of nicotine compared to control rabbits (26 +/- 2% vs. 23 +/- 2% of the left ventricle, respectively), or infarct size (31 +/- 5% vs. 37 +/- 4% of risk zone). Since no effect on infarct size was found, a third group receiving higher dose of nicotine, 320 micrograms/kg (n = 6), was added. Infarct size was not different from the control group (39 +/- 6% of risk zone). Nicotine, given intravenously before ischemic insult, does not protect the myocardium. A "preconditioning-like" effect of nicotine is probably not the mechanism of reduced mortality in smoking patients with myocardial infarction.

Analysis of Variance↗
PubMedDate not supplied

Predicting postinfarction left ventricular dysfunction based on the configuration of the QRS complex and ST segment in the initial ECG of patients with a first anterior wall myocardial infarction.

The objective of the study was to identify patients with anterior wall acute myocardial infarction (AMI) at high risk of postinfarction left ventricular dysfunction (LVD). This study population included all patients admitted with a diagnosis of anterior wall AMI (ST segment elevation of > 1 mm in 2 or more precordial leads) without history or ECG evidence of antecedent AMI,who underwent assessment of left ventricular ejection fraction (LVEF) during emergency hospitalization. ST segment deviation from baseline was measured manually 0.08 s after the J point in all leads. Patients (n = 81) were classified into two groups based on the configuration of the QRS complex and ST segment: ST > 1 mm with preserved (pattern A; n = 60) or distorted terminal QRS (emergence of the J point at a level above the lower half of the R wave or disappearance of the S wave in leads with an Rs configuration; pattern B; n = 21). LVD (LVEF < 40%) was significantly more prevalent in patients with pattern B than pattern A (48 vs. 12%; p = 0.002). There was no correlation between the number of leads with ST segment elevation and LVD (p = 0.47). The sum of ST segment elevation in involved leads correlated weakly, yet significantly with LVEF (R = -0.22; p < 0.05). In conclusion, patients with anterior wall AMI and pattern B in the initial ECG are at high risk of post-AMILVD.

Adult↗
PubMedDate not supplied

Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTO-I (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial Investigators.

BACKGROUND: Ventricular septal defect (VSD) complicating acute myocardial infarction has been studied primarily in small, prethrombolytic-era trials. Our goal was to determine clinical predictors and angiographic and clinical outcomes of this complication in the thrombolytic era. METHODS AND RESULTS: We compared enrollment characteristics, angiographic patterns, and outcomes (30-day and 1-year mortality) of patients enrolled in the Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries (GUSTO-I) trial with and without a confirmed diagnosis of VSD. Univariable and multivariable analyses were used to assess relations between enrollment factors and the development of VSD. In all, 84 of the 41 021 patients (0.2%) developed VSD, a smaller percentage than reported in the prethrombolytic era. The median time from symptom onset to VSD diagnosis was 1 day. Enrollment factors most associated with this complication were advanced age, anterior infarction, female sex, and no previous smoking. The infarct artery was more often the left anterior descending and more likely to be totally occluded in patients who developed VSD. Mortality at 30 days was higher in patients with VSDs than in those without this complication (73.8% versus 6.8%, P<0.001). Patients with VSDs selected for surgical repair (n=34) had better outcomes than patients treated medically (n=35; 30-day mortality, 47% versus 94%). CONCLUSIONS: Compared with historical control subjects, patients who undergo thrombolysis within 6 hours of infarction onset may have a reduced risk of later VSD. If patients develop this mechanical complication, however, it typically occurs sooner than described in the prethrombolytic era. Despite improvements in medical therapy and percutaneous and surgical techniques, mortality with this complication remains extremely high.

Age Factors↗