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Biomedical subjects

L G Futterman

Publications and source records attributed to L G Futterman.

At least 37 records · Page 2Linked to original sources
PubMed1998

Fifty percent of patients with coronary artery disease do not have any of the conventional risk factors.

Prinzmetal's variant angina, primarily a vasospastic disease, is a glaring example of the gaps in our knowledge regarding the etiology of coronary heart disease. Half of all patients with coronary heart disease do not have any of the established coronary risk factors. Prinzmetal's variant angina, syndrome X, coronary embolization, and congenital coronary anomalies, are a few examples of conditions that may not be associated with established risk factors. New risk factors that are emerging in an attempt to establish an etiology in this group of patients are homocysteine plasma fibrinogen, estrogen-deficiency lipoprotein (a), C-reactive protein, Chlamydia pneumoniae, factor VII endogenous tissue plasminogen, and endogenous plasminogen activator/inhibitor type I. The battle against cardiovascular disease continues!

Adult↗
PubMed1998

The ECG in cardiac stress testing: a valuable, but unappreciated source of clues.

The ECG exercise stress test is a very potent aid to the clinical diagnosis of CAD. Thorough knowledge of the ECG abnormalities and clinical features related to the stress test are required for an accurate diagnosis. The ECG exercise stress test is not a substitute for clinical acumen. Proper evaluation of the stress test is a clinical art of the skilled clinician. ECG exercise stress testing can be done efficiently and effectively by trained emergency department physicians. As a result, the diagnosis of CAD can be greatly accelerated.

Adult↗
PubMed1997

Amiodarone: a late comer.

Amiodarone is useful in the treatment of patients with ventricular arrhythmias after acute myocardial infarction and was equally useful when these arrhythmias were associated with CHF. Amiodarone prolongs repolarization and lowers heart rate, actions that are beneficial in treating symptomatic arrhythmias. The absence of proarrhythmic effects distinguishes amiodarone from other antiarrhythmic agents. No excess mortality was seen in any of the amiodarone trials, and in fact, a definite trend toward a decrease in the number of sudden deaths was noted. For many years, amiodarone has been the antiarrhythmic drug of choice in Europe. Only in recent years has this drug gained respectability in the United States. Amiodarone is truly a late comer to our shores.

Amiodarone↗
PubMed1997

SGOT, LDH, HBD, CPK, CK-MB, MB1MB2, cTnT, cTnC, cTnI.

The troponin assay is the "new kid on the block." cTnI is currently the most sensitive, specific marker for cardiac damage and will replace the other less specific cardiac markers. This is a result of continued search for measures that provide the earliest diagnosis, which in turn ensures the greatest positive influence on morbidity and mortality in acute MI. Is the cTnI assay the ultimate marker for cardiac injury? It is doubtful. Only time will tell.

Angina, Unstable↗
PubMed1997

Harnessing the platelet.

Appreciation of the critical role of platelets in cardiovascular disease came when it was shown that aspirin, by virtue of its ability to block platelet aggregation, reduced the combined incidence of MI, stroke, and vascular death by 25%. Understanding the key role played by platelets in acute thrombotic vascular events prompted the development of a new class of drugs to control platelet action. Platelet aggregation is mediated exclusively by the platelet fibrinogen receptor GP IIb/IIIa. The binding of the receptor with fibrinogen is the final common pathway leading to platelet aggregation and thrombus formation. Abciximab, the first GP IIb/IIIa platelet receptor inhibitor, effectively reduces the thrombotic complications in acute coronary vascular events. The newer GP IIb/IIIa inhibitors, the synthetic peptide antagonists, have been shown to be more specific, to be nonimmunogenic, and to cause less bleeding. It is predictable that an oral GP IIb/IIIa inhibitor will become part of the standard repertoire in patients with unstable angina. The platelet has taken center stage in the battle against arterial thrombosis. The direction of our medical attack on acute coronary events is clear: harness the platelet.

Angioplasty, Balloon, Coronary↗
PubMed1997

Sudden cardiac death--preventable--reversible.

SCD is defined as unexpected death due to cardiac causes that occurs within 1 hour of acute symptoms. SCD can be reversed with the use of an ICD. These devices now can be implanted by catheter techniques, obviating thoracotomy. SCD is preventable. The incidence of SCD can be significantly reduced by addressing the fundamental pathophysiology of SCD, which primarily is CAD. Our combined and aggressive implementation of preventive regimens to reduce the risk of cardiac events will save lives. These measures include diet, weight reduction, smoking cessation, regular exercise, and therapeutic drugs. Amiodarone, although effective in preventing lethal ventricular arrhythmias, has not matched the long-term results of the ICD in the successful management of SCD.

Death, Sudden, Cardiac↗
PubMed1996

Management of congestive heart failure: is the role of positive inotropic therapy fading?

Significant strides have been made in the medical therapy of chronic CHF in the past two decades. Treatment has evolved from therapy based on the older concepts of the pathophysiology of CHF to evidence-guided therapy supported by results of major landmark studies that expand the understanding of the pathophysiology. Attenuation of neurohumoral activation is now a goal of pharmacological therapy, and we know that agents that offer hemodynamic and early clinical improvement may not necessarily prolong survival-unless they also modulate these neurohormonal systems. Positive inotropic therapy (e.g., use of a digitalis glycoside) is no longer considered essential in patients with CHF in sinus rhythm. Although impressive hemodynamic benefits can be observed with the use of positive inotropic agents, long-term treatment with these drugs has not produced clinical benefits and may increase mortality. Long before the current concerns about the use of positive inotropic therapy for CHF, cardiovascular physiologists had advised that contractility does not equate with overall cardiac performance. Stimulation of myocardial contractility is a property of digoxin therapy. However, cardiac function is governed by four determinants: preload, afterload, rhythm, and contractility. All four require control. Treatment aimed at reducing preload and afterload and improving arrhythmias can achieve cardiac compensation by reducing cardiac work without the need for digoxin therapy or other inotropic drugs.

Cardiotonic Agents↗
PubMed1995

Presumed consent: the solution to the critical organ donor shortage?

Extraordinary advances in science and medicine such as transplantation of human tissues not only bring about previously unimaginable societal benefits but also create profound implications that involve autonomy and belonging, opposing moral considerations, and legal concerns. Today, technology is changing faster than our values. The issue of salvaging organs from the dead to meet the escalating need for human organs for lifesaving organ transplantation has evolved into an intricate web of interdisciplinary concerns and value conflicts; right and wrong are opinions and consensus does not seem to exist. This organ supply-demand mismatch, as well as suggestions for its resolution, has become a major challenge to the transplant community and to those in political and bioethical arenas. A methodical transition to presumed consent, or opting-out legislation, which removes the burden of decision from the family and the burden of request from the healthcare professional, may be the only solution to correct the imbalance between human organ need and availability.

Ethics, Medical↗
PubMed1995

Sudden death in athletes.

HCM, as well as coronary and myocardial structural abnormalities, is the most common pathology leading to SCD in young athletes. Furthermore, SCD from fatal arrhythmia seems to be the most common mechanism of death. In this population, however, data are insufficient to support either invasive or noninvasive approaches to clarify risk stratification for SCD. Because of the large population, variants of normal found within the athletic population, and the rarity of the disease, screening for individuals at risk is neither practical nor cost-effective. Not all athletes with HCM are at the same risk for SCD; a thorough history and physical examination should alert the health professional to potential risk factors. Efforts are under way to stratify athletes at risk for SCD to determine who can participate in competitive sports and who should not. However, until research can accurately define variables of hemodynamic and electrical instability that permit reliable identification of athletes with HCM who are at risk for SCD, the recommendation is to disqualify athletes with confirmed HCM from moderate- to high-intensity competitive sports. This recommendation includes athletes with or without symptoms or left ventricular outflow obstruction. Due to the decreased risk of SCD in older athletes, individual judgment of eligibility may be used. Athletes thought to have had myocarditis should be withdrawn from all competitive sports for a convalescent period of approximately 6 months, with thorough cardiac assessment and testing performed before returning to training. Athletes with atrial or ventricular tachyarrhythmia must be screened for structural abnormality, heart response during exercise, and the frequency and duration of the arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗