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B D Bertolet

Publications and source records attributed to B D Bertolet.

28 records · Page 2Linked to original sources
PubMed1993

Unstable angina: relationship of clinical presentation, coronary artery pathology, and clinical outcome.

Patients with unstable angina are heterogeneous with respect to presentation, coronary artery morphology, and clinical outcome. Subclassification of these patients based on clinical history has been proposed as a means of identifying individuals at increased cardiac risk. We applied such a classification system to 129 patients discharged from a coronary care unit with a diagnosis of acute myocardial ischemia. Patients were then assessed for cardiac events (recurrent angina requiring revascularization, myocardial infarction, death) 12 months following hospital discharge. Patients were classified as recent onset unstable angina preinfarction (n = 42), crescendo unstable angina preinfarction (n = 48), and unstable angina postinfarction (n = 39). Within each of these groups, the patients were further subclassified based on the occurrence of angina on effort, at rest, or both. No attempt was made to subset patients taking anti-ischemic drugs at the time of clinical presentation to the physician. Coronary angiographic pathology (morphology and number of vessels involved) was similar in the subgroups, but coronary artery thrombus was statistically more likely to be found in patients with crescendo rest angina preinfarction or with frequent anginal episodes at rest postinfarction. Mortality was significantly higher for patients with unstable angina postinfarction (7.7%) than preinfarction (1.1%). No statistical differences were noted between the subgroups with respect to the occurrence of myocardial infarction or recurrent unstable angina requiring revascularization. These data suggest that subclassification of unstable angina patients based on clinical characteristics at presentation is not useful to predict subsequent myocardial infarction or recurrent angina requiring revascularization.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Unrecognized left ventricular dysfunction in an apparently healthy alcohol abuse population.

To examine effects of chronic alcohol abuse on left ventricular function, 162 otherwise relatively healthy alcohol abusers, having been admitted to a rehabilitation program, underwent cardiac evaluation including chest X-ray, electrocardiogram, and radionuclide angiography after 2 weeks abstinence. Twenty-nine of the 162 alcoholic subjects (18%) with left ventricular dysfunction were identified. Twenty-two had regional wall motion abnormalities, suggesting a localized process, of whom 12 also had depressed ejection fractions. Seven others had a depressed ejection fraction alone with a more global myopathic process. Only 4 of these 29 patients had any history suggesting prior heart disease. Two of the 29 had Q-waves greater than or equal to 0.4 s and 8 had an abnormal cardiothoracic ratio on chest X-ray. Chronic alcohol abusers appear to be at relatively high risk for left ventricular dysfunction; most of which is unrecognized. Routine screening methods failed to identify 85% of our subjects who later were recognized by radionuclide angiography. Since historical and electrocardiographic abnormalities are often absent in this population, detection of left ventricular dysfunction by other methods such as radionuclide angiography must be used.

Adult↗
PubMed1990

Unrecognized left ventricular dysfunction in an apparently healthy cocaine abuse population.

To determine the frequency and severity of clinically unrecognized left ventricular (LV) dysfunction related to cocaine use, 84 asymptomatic cocaine abusers underwent cardiac evaluation which included chest x-ray, electrocardiography (ECG), and radionuclide angiography after a two-week abstinence from cocaine use. LV dysfunction was discovered in 6/84 (7%). Regional wall motion abnormalities suggesting a localized myocardial abnormality were found in 2, whereas an ejection fraction less than 50% suggesting a more global process was noted in 4. An abnormal chest x-ray was found in only 1 subject and none had abnormal ECGs. In each of these cases, repeated and protracted use of cocaine was documented and the suggestion of cardiac dysfunction was supported by at least one other independent abnormal finding. In these 6 cases, the dysfunction was clinically unrecognized and unsuspected after routine evaluation. The significance of subclinical LV dysfunction in this population has not been determined and requires long-term study.

Adult↗
PubMed1989

Unrecognized myocardial infarction.

MI is frequently unrecognized for reasons that are unknown, comprising approximately 40 percent of all MIs that occur. Although many unrecognized MIs are accompanied by symptoms of some sort, probably half are totally asymptomatic. Patients with unrecognized MI seem to be similar to those with typical presentations, with similar risk factors and other characteristics. It appears that MI carries the same prognosis whether clinically apparent or not and, therefore, warrants management in both cases. Therapy for silent MI should be aimed at (1) identification and modification of risk factors, (2) identification and treatment of residual ischemia, and (3) attempts at reducing the risk of reinfarction with subsequent morbidity and mortality. As we develop a better understanding of silent ischemic heart disease, hopefully the optimal management strategy for these patients will emerge.

Humans↗
PubMedDate not supplied

Treatment strategies for daily life silent myocardial ischemia: a correlation with potential pathogenic mechanisms.

Recent investigations of SMI occurring during daily life have advanced our understanding of the pathophysiology of myocardial ischemia. These contributions have directed our attention away from "chest pain" alone and physical exertion as the central provoking factor toward transient myocardial ischemia and its broader triggers and consequences. Transient myocardial ischemic episodes, the majority of which are silent, are found in a subset of patients with any clinical manifestations of CAD (eg, stable angina, unstable angina, myocardial infarction, and sudden death), as well as in those patients with CAD who are and have been totally asymptomatic. These episodes are an independent predictor of increased risk for future cardiac events. Most medical therapy and revascularization therapies have the potential to prevent or relieve these silent episodes; however, we do not yet know which method is superior in reducing SMI episodes or preventing future cardiac events. Furthermore, the benefit of reducing SMI versus the cost and potential morbidity of these chosen therapies is not known. At least three trials are now underway to examine some of these concerns (Table 2). Focus on pain relief alone does not appear to be an adequate approach to alter outcome in patients with CAD and may prove insufficient to control SMI. Until these issues are resolved, we believe a conservative approach to the management of patients with CAD is warranted. Documentation of ischemia (painful or painless) is essential. Three general principles should be kept in mind. First, the presence of detectable ischemia is of central importance. This information should be used in the overall risk assessment of the patient. Second, the level of concern or aggressiveness of treatment should be based on the risk associated with the ischemic abnormalities documented (Table 3). The exercise stress test is the most useful to begin this process. The detection of ischemic-type ST-segment depression, either silent or painful, at a low workload (eg, less than or equal to 120 beats per minute or less than or equal to 6.5 metabolic equivalents [METS]) implies high risk for adverse outcome. Likewise, these ST-segment changes occurring in leads that reflect multiple coronary artery distribution, of greater than 2 mm in magnitude and persisting for greater than 6 minutes, are all markers for high risk. Thallium redistribution defects occurring at low work loads, in multiple areas, associated with increased lung uptake and enlargement of the cardiac pool all imply high risk.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic beta-Antagonists↗