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Biomedical subjects

R Berent

Publications and source records attributed to R Berent.

At least 37 records · Page 2Linked to original sources
PubMed2001

Lessons learned from statin trials.

This article aims to review lessons learned about lipid lowering and statins in the past decade and to consider what developments the future may hold. Results from a series of landmark clinical trials confirm that statins significantly reduce cardiovascular morbidity and mortality in patients with and without previous coronary artery disease. The potential of this drug class has yet to be fully explored. Studies currently under way will answer many of the outstanding questions.

Arteriosclerosis↗
PubMed2001

[Acute coronary syndromes: an update. II. Coronary revascularization and risk stratification].

UNLABELLED: CORONARY REVASCULARIZATION: PTCA in patients with refractory unstable angina is associated with a substantial risk of the following complications: death, myocardial infarction, need for emergency surgery, and restenosis. The introduction of intracoronary stents, however, has improved both short-term and long-term outcomes. The newer adjunctive pharmacologic therapies enhance even further the benefits associated with the use of stents. The decision regarding the specific revascularization procedure to be used (e.g., CABG, PTCA, stent placement, or atherectomy) is based on the coronary anatomy, the left ventricular function, the experience of the medical and surgical personnel, the presence or absence of coexisting illnesses, and the preferences of both the patient and the physician. RISK STRATIFICATION: Among patients with unstable angina or non-Q-wave myocardial infarction, there is an increased risk of death within 6 weeks in those with elevated troponin I levels and the risk of death continues to increase as the troponin level increases. Reversible ST segment depression is associated with an increase by a factor of 3-6 in the likelihood of death, myocardial infarction, ischemia at rest, or provocable ischemia during a test to stratify risk. Exercise or pharmacologic stress testing provides important information about a patient's risk. Although the conditions of the majority of patients with unstable angina will stabilize with effective antiischemic medications, approximately 50-60% of such patients will require coronary angiography and revascularization because of the "failure" of medical therapy. High-risk patients are those who have had angina at rest, prolonged angina, or persistent angina with dynamic ST segment changes or hemodynamic instability, and they urgently require simultaneous invasive evaluation and treatment. Medical therapy should be adjusted rapidly to relieve manifestations of ischemia and should include antiplatelet therapy (aspirin, or ticlopidine or clopidogrel if aspirin is contraindicated), antithrombotic therapy (unfractionated heparin or low-molecular-weight heparin), beta-blockers, nitrates, and possibly calcium-channel blockers. Early administration of glycoprotein IIb/IIIa inhibitors may be particularly important, especially in high-risk patients with positive troponin tests or those in whom implantation of coronary stents is anticipated.

Acute Disease↗
PubMed2001

[Acute coronary syndromes: an update. I. Pathogenesis and drug therapy].

BACKGROUND: Unstable angina accounts for more than one million hospital admissions annually. 6-8% of patients with this condition have non-fatal myocardial infarction or die within the first year after diagnosis. Recently, the term "acute coronary syndromes" has been used to describe the spectrum of conditions that includes unstable angina, non-Q-wave myocardial infarction (which generally presents without ST-segment elevation), and Q-wave myocardial infarction (which generally presents with ST-segment elevation). PATHOGENESIS: Disruption of a formed plaque is a complex pathologic process that is central to the initiation of the acute coronary syndromes. Local thrombosis occurring after plaque disruption results from complex interactions among the lipid core, smooth-muscle cells, macrophages, and collagen. TREATMENT: Multiple huge clinical trials confirmed that aspirin reduces the risk of death from cardiac causes and fatal and non-fatal myocardial infarction by about 50-70% in patients presenting with unstable angina. Ticlopidine may be substituted for aspirin in patients with hypersensitivity to aspirin or gastrointestinal intolerance. Clopidogrel acts similarly to ticlopidin but has fewer side effects than ticlopidine and has not been reported to cause neutropenia. High-risk patients with refractory unstable angina and elevated troponin levels may have substantial benefit of glycoptotein (GP) IIb/IIIa inhibition. Current practice guidelines support the use of the combination of unfractionated heparin and aspirin for the treatment of unstable angina. Clinical studies have demonstrated that the incidence of the composite end point of death, myocardial infarction, or recurrent angina was lower with enoxaparin than with unfractionated heparin. Beta-blockers, nitrates, and calcium-channel blockers are useful for antiischemic therapy in patients with acute coronary syndromes.

Acute Disease↗
PubMed2001

Headache as a manifestation of fatal myocardial infarction.

Cardiac ischemia typically causes chest pain, variously radiating elsewhere. Convergence of cardiac nerve fibers on central pathways receiving somatic afferents from the head is likely to be responsible for the perception of cardiac ischemic pain as headache. A 47-year-old man was admitted to the emergency room of our hospital with a 2-hour history of occipital headache. Routine electrocardiography revealed monophasic ST-segment elevation in leads I and aVL and ST-segment depression in leads II, III, and aVF. During recording of lead VI, ventricular fibrillation occurred. Advanced life support was started immediately but failed to restore rhythm and cardiac function. Autopsy showed two-vessel disease with a ruptured plaque and total thrombotic occlusion of the proximal left anterior descending artery and 80% stenosis of the right coronary artery. In this patient, headache was the only symptom of myocardial ischemia. Anatomic convergence of cardiac nerve fibers on central pathways receiving somatic afferents from the head is likely to be responsible for the perception of cardiac ischemic pain as headache. Owing to the very rare occurrence of headache as a symptom of myocardial ischemia, diagnosis is difficult and requires a high degree of suspicion.

Coronary Artery Disease↗
PubMed2001

[Coronary artery bypass graft dysfunction--clinical presentation, laboratory and electrocardiographic parameters].

The recurrence of symptoms after coronary artery bypass surgery is often caused by bypass-dysfunction. In this study we tried to determine factors related to the long-term patency of arterial and venous bypass grafts. We evaluated all patients with bypass grafts undergoing coronary angiography in the year 1998 at our hospital (163 patients, mean age 67 years, mean interval since the operation 79 months, a total of 341 venous bypasses (VBP), 386 peripheral venous anastomoses and 85 arterial (LIMA = left internal mammarial artery) bypasses. The data were collected by a retrospective analysis of the hospital records. Statistics were performed using the Wilcoxon-Mann-Whitney-U test. After an interval of 53 months LIMA-bypasses were patent without stenosis in 92%. Symptoms were caused in only 2% by a dysfunction of the LIMA-graft. The patency of venous bypass grafts decreased with time (5 years after the operation 74% were patent without stenosis, 5-10 years 56%, more than 10 years 35%, p < 0.01). We found clear relations between the function of the venous grafts and the clinical presentation (patent grafts without stenosis in 43% with acute coronary syndromes, in 57% with stable angina [p = 0.08] and in 86% with atypical angina [p < 0.0001 for the difference between each of the first two and the last syndrome]), the resting-ECG (65% patent VBP without stenosis with normal ST-segments and 49% with abnormal ST-segments, p < 0.01), the body-mass-index (70% patent VBP without stenosis with a BMI < 25 and 56% with a BMI > 30, p = 0.05) and the erythrocyte sedimentation rate after 2 hours (79% patent VBP with an ESR < or = 20 mm vs. 64% with an ESR > 49 mm, p = 0.02). The function of VBP after coronary artery bypass graft (CABG)-procedure depends primarily upon the interval since the operation. In addition, we found correlations with clinical presentation, resting-ECG, body-mass-index and erythrocyte-sedimentation rate as a possible marker of inflammation in bypass-atherosclerosis. Therefore, inflammatory processes seem to play an important role in the development of venous graft dysfunction.

Aged↗
PubMed2001

[Pathophysiology and therapeutic aspects of left ventricular "remodeling" in the post-infarct phase].

Left ventricular remodeling is the process by which ventricular size, shape, and function are regulated by mechanical, neurohormonal, and genetic factors. Remodeling may be physiological and adaptive during normal growth or pathological due to myocardial infarction, cardiomyopathy, hypertension, or valvular heart disease. Postinfarction remodeling has been divided into an early phase within 72 hours and a late phase beyond 72 hours. The early phase involves expansion of the infarct zone, which may result in early ventricular rupture or aneurysm formation. Late remodeling involves the left ventricle globally and is associated with time-dependent dilatation, the distortion of ventricular shape, and mural hypertrophy. Hypertrophy and collagen degradation are adaptive responses during postinfarction remodeling. Myocardial repair is triggered by cytokines released from injured myocytes. Ventricular remodeling is influenced most by infarct artery patency. Once infarct evolution has occurred, pharmacological intervention, like ACE inhibition and beta-adrenoreceptor blocking agents, may minimize infarct expansion and ventricular dilatation and improve the long-term prognosis.

Humans↗