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Biomedical subjects

L G Futterman

Publications and source records attributed to L G Futterman.

At least 19 recordsLinked to original sources
PubMed2001

Lp(a) lipoprotein--an independent risk factor for coronary heart disease after menopause.

Lp(a) is an independent risk factor for recurrent atherosclerotic heart disease in men and women after menopause. Excess levels of Lp(a) are seen in both males and females, more common in Africans, African Americans, and Asian populations than in whites. Since the standard lipid profile does not report Lp(a), it has to be ordered separately. Screening for Lp(a) should be considered under the following circumstances: (a) patient or family history of premature atherosclerotic heart disease, (b) familial history of hyperlipidemia, (c) established atherosclerotic heart disease with a normal routine lipid profile, (d) hyperlipidemia refractory to therapy, and (e) history of recurrent arterial stenosis. Treatment options are (a) a new extended-release form of niacin 3 to 4 g daily (although most effective in lowering Lp(a) and in reducing atherosclerotic heart disease mortality rates, its use may be limited because of side effects); (b) estrogen replacement after menopause, (however, concomitant progesterone therapy dilutes the effectiveness of estrogens); (c) lowering LDL with statins (generally effective in atherosclerotic heart disease but has no effect on Lp(a) levels), (d) aspirin and antibiotics (may be effective when C-reactive protein levels are high); and (e) folic acid (reduces homocysteine levels). The general measures that halt the progression of CAD should always be adhered to, namely, maintaining normal weight, a daily exercise program, blood pressure control, a low-cholesterol-forming diet, and daily aspirin.

Adult↗
PubMed2001

The mysteries of the human genome uncovered--medicine is changed forever.

It is impossible to overemphasize the significance of the recent announcement that 85% of the DNA of the human genome has been decoded. Physicians can now begin teasing out the secrets of human health and disease. Within the next 10 years, it may be possible to determine who may be vulnerable to illnesses like Alzheimer's disease, cancer, and diabetes. The world of medicine will be utterly transformed in a few decades. Even before decoding of the human genome is completed, scientists have begun a new and more challenging research in explaining the molecular basis of life. "Proteonomics," the cataloging and analysis of every protein in the human body looms as the next major scientific medical effort. Proteins are more varied and complex than DNA. Fifty years from now, our understanding of the human organism and its various ills will be transformed beyond recognition through genomics and proteonomics. Stay tuned!

Disease Management↗
PubMed2001

Heart failure: update on treatment and prognosis.

HF is a prevalent and debilitating disease, affecting nearly 5 million patients and perhaps an equal number with asymptomatic left ventricular dysfunction who are at high risk of atrial fibrillation developing. An estimated 550,000 new cases occur every year. HF is the most common diagnosis in hospitalized patients aged 65 and over and is a major cause of death. The median survival after onset is 1.7 years in men and 3.2 years in women. The majority of cardiac deaths in patients with HF are sudden and arrhythmogenic: the rest are due to progressive hemodynamic deterioration. A significant advance in the past decade has been the recognition of the importance of inhibiting the neurohormonal action in HF with the use of beta-blockers, angiotensin receptor, and aldosterone antagonists. In addition, a new concept in HF therapy has evolved. The view that chronic HF is an irreversible, end-stage process is being supplanted by the fact that it is possible to effect biological improvement in the intrinsic defects of function and structure in hearts afflicted with chronic HF. Reversibility of HF has been reported by (1) unloading the failing heart using an LVAD, (2) the sophisticated use of diuretic combinations and neurohormonal blocking drugs, or (3) employing continuous arteriovenous hemofiltration. Thus it is now possible to reverse a process that has long been considered irreversible. Exercise programs designed for patients with HF that have been advocated recently can be difficult to apply. Fine tuning of an exercise regimen is required because a reduction in cardiac work is mandatory when treating HF, where the concern is that the heart may not be capable of supplying the metabolic needs of the body, even in resting states. Finally, although not emphasized in the recent literature on HF, the use of diuretics and sodium restriction continue to be the mainstays of therapy without which compensation of HF is not possible.

Adrenergic beta-Antagonists↗
PubMed2001

Brugada.

The Brugada syndrome was first described in 1992. Palpitations and/or syncope are usually experienced during rest and increased vagal activity. [table: see text] However, in 15% of patients with Brugada syndrome, symptoms occur during physical activity. The syndrome is further characterized by a pattern of RBBB and ST-segment elevation in V1 to V2/V3 (see Table). One major and one minor criterion from the Table can serve to establish a diagnosis of Brugada syndrome. The patient presented in this report described symptoms only during physical activity. EPS confirmed the diagnosis of the Brugada syndrome, and an ICD was implanted. The clinical importance of the Brugada syndrome is that it calls attention to patients at risk for SCD. The syndrome is genetically determined and caused by mutations in the cardiac ion channels. Signal averaging that reveals late potentials can help identify persons who may be at high risk for SCD and who would thus be candidates for EPS, which can identify those at risk of SCD. The ICD is the only therapy known to help prevent SCD in patients with Brugada syndrome.

Adult↗
PubMed2000

Update on management of acute myocardial infarction: facilitated percutaneous coronary intervention.

Combination therapy with abciximab and reteplase and heparin allows high rates of patency 60 minutes after therapy. PTCA is facilitated by these adjunctive therapies to improve procedural outcomes. Stent implantation and blockade of the platelet GP IIb/IIIa receptor with abciximab provide potent complementary benefits allowing PTCA to be performed at a new standard of safety and efficacy. Thus the acronym FPCI stands for the use of drugs, angioplasty and stenting. Time and experience will determine the efficacy of the combined pharmacological-mechanical bridge. We believe that FPCI is the wave of the future and that in skilled hands this emergent coordinated care of acute MI has lowered and will continue to lower morbidity and mortality in acute coronary events.

Abciximab↗
PubMed2000

The Framingham Heart Study: a pivotal legacy of the last millennium.

The life span at birth in the Greco-Roman era (200-300 BC) was 27 years. The life span in 1900 was 47 years, representing a gain of 20 years in more than 2000 years, or an increase of 1 year per century. At the close of the 20th century, the average life span was 77 years. This is a 30-year gain in life expectancy in only 1 century, or an average of 3 years for every decade in the last century. Compare that with only 1 year gain in life expectancy per century for the previous 20 centuries. It must be quite evident from this brief review that in the last century the Framingham Heart Study played a pivotal role in influencing physicians and the public to place major emphasis on the prevention of CV disease. To be sure, the control of epidemics, cure of infections with antibiotics, universal vaccination, and establishing food and environmental safety standards in the last century were instrumental in extending the life span. Nevertheless, major and direct influences on the explosive expansion in longevity during our life time were the contributions of the Framingham Heart Study. To paraphrase W. B. Kannel, a chief investigator in the Framingham Heart Study, "A cardiovascular event should be regarded as a medical failure rather than the first indication for the need to treat."

Adult↗
PubMed2000

A novel device in evaluating syncope.

Syncope may be a manifestation of many diseases. The etiology is often difficult to determine. Much effort, time, and expense have been required to determine a diagnosis. A thorough history and physical examination are essential (Table 3). Several clinical pearls may be of help in the diagnosis of syncope: (a) the most important elements in the evaluation of syncope are a detailed history and physical examination; (b) syncope is a common problem in young healthy adults and the elderly; (c) a heavy meal is a specific cause of syncopy in the elderly (postprandial), however this etiology often goes unrecognized; (d) syncope is caused by 1 of 3 mechanisms: decreased cardiac output, systemic vascular resistance, or cerebrovascular disease; (e) reflex-mediated syndromes (vasovagal) are common causes of syncope in young adults, and orthostatic hypotension is an important cause of syncope in the elderly; and (f) the 1-year mortality of cardiac syncope (18%-33%) is significantly higher than that from non-cardiac syncope (0%-12%). A proven and useful tool has recently been advanced to aid in the evaluation of syncope. The Reveal Plus insertable loop recorder has auto activation that allows automatic capture and recording of arrhythmic events. Patient activation is an option. The recorder lasts 12 to 14 months and has proven to be a valuable and reliable cost-effective asset in our quest to evaluate syncope.

Adult↗
PubMed2000

Peripartum cardiomyopathy: an ominous complication of pregnancy.

PPCM is a relatively rare and lethal disease, poorly characterized and about which little is known. A diagnosis is made within a confined narrow period, the ninth month of pregnancy to the fifth month postpartum. The signs and symptoms of heart failure are classic, and failure is confirmed by an echocardiogram primarily showing either hypertrophy or dilatation and a low ejection fraction. Other causes of heart failure should be ruled out before the diagnosis of PPCM is made. Treatment is supportive and similar to standard therapy for heart failure. Probabilities of atrial or ventricular emboli are similar to the other dilated cardiomyopathies in heart failure and are treated accordingly, i.e., with coumadin or enoxaparin. Since mortality rates are high and can be between 18% and 56%, heart transplantation has been performed and prognosis improved. Finally, immunosuppressant therapy has been used successfully in only a small number of patients who were unimproved after 2 weeks of standard therapy.

Adult↗
PubMed2000

Hibernating myocardium, stunning, ischemic preconditioning: clinical relevance.

Hibernation is a chronic condition that can be due to either chronic low perfusion or repetitive stunning. When oxygen demands increase, prolonged periods of ischemia occur, resulting in multiple episodes of stunning. Because hibernation may play a significant role in refractory failure, the diagnosis of hibernation followed by reperfusion can be life saving. Myocardium that has sustained a transient sublethal injury but has the potential for recovery with time is referred to as stunned myocardium. Myocardial stunning is commonly seen after coronary artery bypass surgery: variable periods of myocardial ischemia are sustained during coronary artery bypass graft surgery, and when these patients return to the intensive care unit, their ventricular function is severely impaired because of the prolonged anoxia during bypass. With the support of artificial assist devices, counterpulsation or temporary use of catecholamines, these patients improve and have a favorable prognosis. Similarly, recovery occurs with time in stunning that follows AMI or cardiac transplantation because in either case the heart had been temporarily anoxic. Clinical observations of ischemic preconditioning include the following: (1) first-effort angina or "warm-up phenomenon," i.e., angina with exercise early, but similar or greater effort the rest of the day does not cause any angina and (2) mortality of AMI is lower in patients with a history of angina preceding AMI. Angina 1 to 2 hours before AMI is the most effective time window for ischemic preconditioning. A less potent "second window" is observed when angina occurs during the second to fourth day before AMI. Adenosine possesses marked cardioprotective properties and has been used to pharmacologically induce ischemic preconditioning with some success. Work is still in progress.

Adenosine↗
PubMed1999

The use of antioxidants in retarding atherosclerosis: fact or fiction?

The proposal that antioxidants may retard the progression of atherosclerosis is not new. Published studies examining the effect of antioxidants on experimental antioxidants extend back to 1940. The results have all been inconsistent. However, the data regarding the beneficial effects of retarding atherosclerotic progression are strong enough to warrant continued research on the lipoprotein oxidation theory or atherosclerosis. However, caution is needed to avoid embracing a concept without proof. It should be noted that the National Cholesterol Education Program does not recommend the use of antioxidant vitamin supplements to reduce CAD. Atherogenesis is produced by multiple factors. To believe that all such factors are mediated by uncontrolled oxidative events is, to say the least, naive. Finally, should antioxidants prove to be effective in retarding coronary atherosclerosis, their place on the therapeutic ladder of CAD prevention would be low. The overwhelmingly proven evidence favors the following factors that have been proven to lower morbidity and mortality due to atherosclerosis: (a) treatment of hypertension, (b) cessation of tobacco use, (c) treatment of dyslipidemia, (d) achieving a normal weight, (e) regular exercise, (f) treatment of homocystinuria, especially in cases with renal disease, and (g) antioxidants.

Antioxidants↗
PubMed1999

Commotio cordis: sudden cardiac death in athletes.

Commotio cordis due to blunt trauma to the precordium is a rare cause of death in young athletes, occurring less frequently than all of the other athletics-related deaths. Several measures, such as the use of safety baseballs and the use of chest protectors, can help protect young athletes from commotio cordis. In general, sudden cardiac death in athletes is receiving increasing attention from the public as a result of recent deaths of high-profile athletes. Sudden cardiac death, however, is rare, with an estimated 1 out of 200,000 high school athletes at risk each year. However, the personal, physiological, and cardiovascular benefits of athletics far outweigh the risks. Therefore, the message to parents is to allow their children to participate in athletics because the benefits far outweigh the risks.

Adolescent↗
PubMed1999

Stroke risk, cholesterol and statins.

The natural statins should be used as first line agents in the prevention of stroke. The effects of the synthetic statins on the prevention of coronary events and stroke have not been reported at this time. The National Stroke Association's Stroke Prevention Advisory Board has prepared a consensus statement on risk reducing intervention. The Board identified hypertension, MI, atrial fibrillation, hyperlipidemia and asymptomatic carotid artery stenosis (60% to 99% occlusion) as proven stroke risk factors. The Board's recommendations for the prevention of a first stroke are: 1. Hypertension should be treated with lifestyle, pharmacologic and multidisciplinary management strategies. 2. Aspirin post MI and warfarin (international normalized ratio, 2 to 3) for patients with atrial fibrillation, left ventricular thrombus or significant left ventricular dysfunction. Statin agents should be used post MI. 3. Atrial fibrillation patients age 75 or older should be treated with warfarin. Younger patients 65 to 75 with atrial fibrillation and risk factors should be treated with warfarin [corrected]. Younger patients 65 to 75 with atrial fibrillation without risk factors should be treated with warfarin or aspirin [corrected]. 4. Patients with hyperlipidemia and coronary artery disease should be on statin agents. 5. Carotid endarterectomy is recommended for asymptomatic carotid stenosis (60% to 99%) when surgical morbidity and mortality are less than 3%. 6. Adherence to a low-fat diet, smoking avoidance, mild alcohol use, and physical activity should follow published guidelines.

Aged↗
PubMed1999

Low-molecular-weight heparin: an antithrombotic agent whose time has come.

LMWH (enoxaparin) should be used in combination with aspirin in the early phase of non-Q wave MI and in patients with unstable angina. The benefit of LMWH in acute coronary syndromes has been validated in several clinical trials. In addition, the use of LMWH is cost-effective when compared with use of UFH. The incidence of minor bleeding may be greater with LMWH than with UFH, most frequently due to ecchymosis at the injection site. However, the frequency of major bleeding did not differ between the two heparins. LMWH has been used successfully for the past 4 years by orthopedic surgeons in the prevention of pulmonary emboli. LMWH should replace UFH in the management of acute coronary syndromes.

Angina, Unstable↗
PubMed1998

Sudden death in athletes: an update.

The athlete projects the ultimate image of well-being in the health status spectrum. Nevertheless, exercise-related sudden cardiac death (SCD) is an uncommon, yet tragic, occurrence. Exercise-related SCD is defined by symptoms that arise within 1 hour of participation in sport. The major mechanisms involved in exercise-related SCD are related to haemodynamic and electrophysiological changes brought about by exercise in the susceptible individual. Fatal arrhythmia seems to be the most common mechanism of death. Between 1 and 5 cases of SCD per 1 million athletes occur annually. In young athletes (<35 years old), the majority of these cases are caused by defined and hereditary cardiovascular disorders. Among other aetiologies, hypertrophic cardiomyopathy and coronary artery anomalies are most common in this group. In older athletes (>35 years old), sudden death is usually associated with atherosclerotic cardiac disease. A problem for identifying athletes at risk for SCD is that the athlete's heart undergoes adaptive changes in response to regular physical exercise. Alterations in cardiac function influence the physical examination, the electrocardiogram and the echocardiogram. Because of these characteristic 'abnormalities' of the athlete's heart, it is often difficult to distinguish physiological adaptations from pathophysiological processes. Although studies and observations have helped to clarify the cardiovascular pathology responsible for SCD in young, apparently healthy individuals, effective methods for preventing SCD and identifying and screening athletes at risk remain elusive. Problems with routine comprehensive screening of athletes include the limitations inherent in the predictive value of available diagnostic procedures and the cost of testing large populations. The variation from normal cardiac physiology found within the athletic population and the rarity of SCD in athletes means that elaborate screening to determine individuals at risk is neither practical nor cost effective. A thorough assessment of pertinent family and medical histories, cardiac auscultation of young athletes, evaluation of exercise-induced symptoms and education of older athletes to the symptoms of cardiac ischaemia are all essential to primary prevention of SCD in the athletic population. Until reliable methods can accurately identify those athletes at risk for SCD, broad recommendations are available to help guide the management and participation in sports of athletes with cardiovascular disease.

Adaptation, Physiological↗
PubMed1998

Inflammation in plaque rupture: an active participant or an invited guest?

Numerous reports have established the association of inflammation with acute coronary events. Data have been presented that suggest that elevated levels of CRP indicate heightened risk of future MI and stroke. Thus CRP measurement is both predictive and prognostic of cardiovascular and cerebrovascular events. Is inflammation merely a marker, an invited guest so to speak, or is inflammation an active participant that influences the process of plaque rupture and thrombus formation? The beneficial effects of aspirin in reducing the risks of a first MI and stroke are directly related to high plasma concentrations of CRP, whereas small, nonsignificant reductions in risk occurred among patients with low or normal CRP levels. Thus inflammation is not only an uninvited guest but is actually an aggressive participant in the destabilization of the atheromatous endothelial plaque.

Coronary Artery Disease↗