Regular physical exercise reduces cardiovascular risks.
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Biomedical subjects
Publications and source records attributed to Laurie G Futterman.
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The clinical use of mild hypothermia to preserve ischemic cardiac and cerebral tissue continues to grow in popularity. This is a result of the known fact that hypothermia reduces myocardial oxygen demands more than any other intervention. The Advanced Life Support (ALS) Task Force of the International Liaison Committee on Resuscitation (ILCOR) made the following recommendations a year ago, in October 2002: "Unconscious adult patients with spontaneous circulation after out-of-hospital cardiac arrest should be cooled to 32 degrees C to 34 degrees C for 12 to 24 hours when the initial rhythm was VF," or in-hospital even when arrest is due to other rhythms. Therapeutic use of hypothermia is in progress.
The edematous states, specifically those in CHF and cirrhosis of the liver, are associated with excessive aldosterone secretion and represent states of secondary hyperaldosteremia. Aldosterone promotes sodium retention by the renal tubules. Spironolactone, first introduced 50 years ago (1953), blocks the action of aldosterone on renal transport of electrolytes, thus acting as an effective diuretic, and in addition, has potentiating effects on other diuretics, including the thiazides. Spironolactone has undesirable side effects that have limited its clinical use; the most significant are impotence, gynecomastia, and hirsutism. Eplerenone, a recently introduced selective ARA, decreases morbidity and mortality in patients with CHF following MI and has none of the androgenic or estrogenic side effects of spironolactone. Eplerenone is an effective alternative for spironolactone.
Accumulating evidence from clinical trials and basic research indicates that statin therapy favorably influences a number of diverse clinical events through both effects related to lowering of LDL cholesterol levels and effects independent of the lowering of LDL cholesterol levels. The latter effects are referred to as pleiotropic. The full potential of this exciting class of drugs in vascular and nonvascular protection is only just being realized. The pleiotropic effects of the statins improve vascular relaxation, promote new vessel formation, and stabilize unstable plaques. Statins reduce glomerular injury, renal disease progression, insulin resistance, and bone resorption. Ezetimibe, a recently approved medication, enhances the lipid-lowering effects of the statins by lowering LDL and increasing HDL levels through its property of inhibiting absorption of cholesterol in the small intestine. These salutary effects of ezetimibe on statin levels presumably enhance the beneficial effects attributed to statin pleiotropy. It is noteworthy that the pleiotropic properties of the statins have been beneficial in a variety of diseases that involve a number of organs and organ systems. No other therapeutic agent can claim equally stellar results in such a wide variety of diseases. The common denominator in all of the diseases that have been shown to improve with statin pleiotropy could be arteriolar pathology due to hyperlipidemia, which improves in response to statins by a return of arteriolar function to normal rather than through statin pleiotropy. Recent reports indicate that higher doses of statins reverse atheromatous changes in the coronary artery when the LDL cholesterol level is lowered to well below 2.59 mmol/L (100 mg/dL). These results lend additional support to the probability that similar pathological changes that may be present in the small arteries and arterioles also can respond to adequate statin therapy. Statin pleiotropy: fact or fiction?
Deep vein thrombosis and its potentially fatal complication, PE, accounts for more than 250,000 hospitalizations annually in the United States. Pulmonary embolism is the most serious complication and has a 3-month mortality of 17%. Two million people each year are affected by VTE, and the prevalence is rising because of the aging population. Deep vein thrombosis and its potential complication, PE, is preventable. However, there still is widespread failure to screen, diagnose, and initiate prophylactic therapy in patients at risk. This failure can be corrected by development of a heightened awareness of risk factors among emergency department physicians and nurses and by similar personnel caring for bedridden hospitalized patients. A recent landmark study Prophylaxis in Medical Patients With Enoxaparin Study (MEDENOX) revealed the risk factors of VTE in order of frequency: (1) previous VTE, (2) acute infectious disease, (3) cancer, (4) age greater than 75 years, and (5) chronic respiratory disease. This study confirmed the effectiveness of a LMWH, enoxaparin, in the prevention of VTE.
All adults have stem cells in their body that can act like embryonic stem cells when given an appropriate stimulus. When VEGF is given, the bone marrow is stimulated to release stem cells, which grow new coronary arteries and also replenish damaged or dead cardiomyocytes. Transplanting autologous bone marrow stem cells into coronary arteries reduced infarct size, improved the prognosis following an acute MI and in patients with chronic congestive heart failure. Since patients are the source of their own stem cells, there would be a ready supply, with no rejection or immunological issues, and political debate on stem cell research would end. It is worth noting that statin therapy stimulates mobilization of EPCs, which repair damaged or dead myocardial cells and stimulate growth of new coronary arteries.
In the past era, we held high-grade arterial stenosis responsible for the acute complications of atherosclerosis. These concepts are being reassessed. Qualitative rather than quantitative aspects of plaques (e.g., inflammation rather than plaque size) have been established as decisive determinants of their probabilities to cause acute complications. Numerous beneficial effects of statins have been demonstrated. These include lipid lowering, plaque stability, enhanced endothelial function, and antiplatelet, antiatherothrombotic, and antimacrophage activities. However, the successful medical management of CAD is also multifactorial and in addition to use of statins include beta-blockers, ACE inhibitors, and aspirin, as well as blood pressure control, diet, and exercise (see [figure: see text] Figure). The results have been not only the preventions of acute complications of atherosclerosis, but also the successes in stabilizing acute coronary events and preventing infarctions.
Inflammation of the coronary arterial wall plays a major role in atherosclerosis and ultimately thrombosis by contributing to vascular constriction, spasm, and thrombus formation. Measurement of hs-CRP level is a readily available laboratory blood test that serves as a gauge of coronary plaque inflammation. As a result, hs-CRP has become a very useful biological marker for predicting the risk of acute coronary events and for making decisions regarding treatment. It is important to recognize that lipid-lowering therapy decreases plaque inflammation and slows the progression of calcium buildup in the coronary arteries, which is readily verified by reduction in hs-CRP levels. Endothelial dysfunction is a product of plaque inflammation and as such can predict acute CV events. Endothelial function can be assessed during cardiac catheterization by measuring the vasoactive response to pharmacological or physiological stress. However, the routine use of cardiac catheterization to measure drug-induced coronary vasoactivity can have potential adverse effects in patients with unstable coronary disease. Time and costs can also be additional constraints in the routine use of this procedure. Consequently the simple and readily available hs-CRP test is accurate and preferable.
Dietary sodium restriction and diuretics are basic requirements in the treatment of CHF. The reduction in pulmonary venous congestion following the use of diuretics leads to a rapid improvement in dyspnea, promotes natriuresis without direct positive inotropic effects, and does not reflexively activate the neuroendocrine system. The recent literature has been replete with reports on the treatment of HF. However, very little has been said about the importance and the methods of use of diuretics in HF. Treatment of HF cannot succeed without regard for the role of the sodium ion in HF. There are nearly 5 million cases of HF in the United States. More than 500,000 new cases are diagnosed each year. Hospital discharges and deaths due to HF have increased more than 100% in the past 2 decades with a 5-year mortality rate close to 50%. Since the leading cause of HF in Western countries is ischemic heart disease, aggressive therapy to halt progression of coronary atherosclerosis can have a major impact on controlling and often curing HF.
The age association and alterations in vascular structure and function at both the cellular and molecular levels are increasingly recognized as major risk factors for CV disease. The arterial remodeling during aging that may be enhanced by the CV risk factors are supersensitive to the age-related risk factors. The aging process may well be influenced by a combination of hereditary and environmental factors. Much can be done to modify environmental risk factors, very little to genetics except for choosing your parents.
Syncope may be related to a large spectrum of medical and psychologic disorders, yet the precise etiology is often difficult to determine. Although the evaluation of syncope involves extensive testing, nearly 50% of these individuals remain without definitive diagnosis. Because of the infrequent and unpredictable nature of syncope, many ambulatory screening techniques are not suited to diagnose syncope. The use of an implantable loop recording device provides continuous monitoring of heart rate and rhythm during syncopal events and may help clinicians arrive at a more precise diagnosis in a more timely manner. The Reveal Plus implantable loop recorder (ILR) (Medtronic USA, Minneapolis, Minn) has demonstrated its clinical utility in evaluating syncope and drug-refractory seizure disorders.