Assad Movahed

Reversible Cardiomyopathy Due to Selenium Deficiency

Selenium is an essential trace element and a component of glutathione peroxidase, an enzyme that may help to prevent oxidative damage to cells. Selenium deficiency has been linked to the development of Keshan disease, a dilated congestive cardiomyopathy occurring primarily in children living in rural China. Sporadic cases have been reported in the United States in individuals with poor nutritional intake, mostly in individuals on long-term home parenteral nutrition. This report describes a young black woman with Crohns disease in whom a congestive cardiomyopathy developed and was subsequently reversed following administration of selenium.

Use of Antihypertensive Drugs during Pregnancy and Lactation

The decision to treat elevated arterial pressure in pregnancy depends on the risk and benefits imposed on the mother and the fetus. Treatment for mild-to-moderate hypertension during pregnancy may not reduce maternal or fetal risk. Severe hypertension, on the other hand, should be treated to decrease maternal risk. Methyldopa and beta-adrenoceptor antagonists have been used most extensively. In acute severe hypertension, intravenous labetalol or oral nifedipine are reasonable choices.

Norepinephrine-induced left ventricular dysfunction in anesthetized and conscious, sedated dogs

These studies were conducted to evaluate effects of high dose norepinephrine infusion on left ventricular function in anesthetized and conscious dogs. Separate groups of pentobarbital anesthetized closed-chest dogs received norepinephrine infusion for 90 min followed by 1 h of recovery. Arterial pressure, electrocardiogram, two-dimensional echocardiogram and an equilibrium radionuclide angiogram were monitored. One hour following infusion of norepinephrine, left ventricular ejection fraction was reduced in a dose-dependent fashion. Fractional shortening was similarly reduced, with increased left ventricular systolic and diastolic dimensions also observed. Left ventricular end-systolic wall stress was increased at 60 min following infusion of norepinephrine but not saline: saline, 68 +/- 8, norepinephrine, 4 micrograms/kg/min, 113 +/- 8 g/cm2. The left ventricular end-systolic wall stress/fractional shortening relationship showed reduction of contractility. In 10 conscious dogs pretreated with morphine, norepinephrine at 5 micrograms/kg/min x 90 min produced similar changes to those seen in anesthetized animals. Ejection fraction was reduced from 0.69 +/- 0.3 to 0.36 +/- 0.04 at 60 min post infusion. Fractional shortening was also reduced. Left ventricular end-diastolic dimension was increased. However, when animals were followed for 1 week, complete recovery occurred within 48 h. Histology showed mild contraction band necrosis in acute experiments and mild perivascular fibrosis in chronic experiments. Therefore, norepinephrine cardiotoxicity produced significant left ventricular dilation and reduction of ejection phase indices of left ventricular function associated with reduced contractility. In chronic dogs, histologic changes were mild, and left ventricular dysfunction was reversible.

Use of cardiovascular medications in the elderly

Cardiovascular disease is the leading cause of death in patients aged 65 and above. Although elderly persons represent only 12.4% of the US population, they account for about a third of drug expenditures. However the appropriate use of cardiovascular medications in these patients has been shown to reduce the rate of cardiovascular morbidity and mortality. The normal aging and the disease process in the elderly result in significant changes at the structural and molecular level in the elderly. The changes that take place in the autonomic nervous system, the kidneys, and the liver in the elderly modify the metabolism and clinical effects of most medications. Elderly patients are also susceptible to side effects and adverse drug reactions. Physicians should have a clear understanding of the normal aging processes, the abnormal changes due to disease process and the changes in the pharmacology of drugs in the elderly to deliver proper care to the elderly patient.

Aortic atheromas: current concepts and controversies-a review of the literature.

The frequent use of transesophageal echocardiogram (TEE) has led to the increased recognition of aortic atheromas. Retrospective and prospective follow‐up studies have reported an association between aortic atheromas and stroke in the high‐risk patient population, with complex plaques being more likely to embolize than simple plaques. However, TEE‐based studies in the low‐risk cohorts have failed to show a similar association. There is growing body of evidence suggesting that aortic atheroma is a marker of generalized atherosclerosis. Although magnetic resonance (MR) imaging and computed tomography (CT) scan are emerging as a powerful noninvasive tool for characterization of aortic atheromas, TEE is the imaging modality of choice. Currently, treatment of aortic atheromas is not well defined, and mixed outcomes have been reported for anticoagulation therapy with warfarin. Statins appear promising based on their plaque stabilization properties. However, there are no randomized control trials to establish the role of both anticoagulation and statins in patients with aortic atheromas, and are warranted in the future.

Inflammation in high blood pressure: a clinician perspective

Hypertension is one of the most important contributors to atherosclerosis. A possible link between inflammation and elevated blood pressure has been suggested by several cross-sectional and longitudinal studies. Possible mechanisms include an imbalance between vasoconstrictors and vasodilators, amplified thrombogenesis and platelet activation, and perhaps a direct effect of inflammatory mediators. C-reactive protein (CRP), an inflammatory cytokine, may play an essential role in vascular inflammation and can directly decrease the production of nitric oxide, a vasocodilator. Angiotensin II (Ang II) up-regulates several inflammatory cytokines, leukocyte adhesion molecules, and chemokines through the activation of the nuclear factor-kappa B leading to a decrease in the bioavailability of vasodilators. The increase in oxidative stress and endothelin-1 production through Ang II may further contribute to vasoconstriction. Adipose tissue can add to the production of CRP and creates a prothrombotic state. The presence of low-grade inflammation, especially elevations of CRP, can help predict the risk of future cardiovascular events and is associated with target organ damage in hypertensive individuals. Angiotensin converting enzyme inhibitors, angiotensin receptor blockers, beta-adrenoreceptor antagonists, and, to a lesser degree calcium channel antagonists, have shown efficacy in reducing CRP. Lifestyle changes such as exercise, weight loss, and tobacco cessation have also shown a similar efficacy. Whether targeting inflammation in the treatment of uncomplicated hypertension can alter the natural history of the disease or lead to improved outcome has yet to be determined.

Uptake of technetium 99m HDP in cardiac amyloidosis.

We present a report and a brief summary of literature focused on a patient with suspected cardiac amyloidosis from transthoracic echocardiography and tc-99m HDP scintigraphy. Imaging demonstrated significantly increased uptake of the bone tracer within the myocardium in comparison to the highest skeletal uptake. Literature described several cases of abnormal myocardial uptake of various imaging tracers in various disease states.

Dobutamine and improvement of regional and global left ventricular function in coronary artery disease.

Abstract The effects of dobutamine infusion on left ventricular (LV) function in patients with coronary artery disease (CAD) have not been completely defined. Some studies have suggested that dobutamine infusion can be used to achieve a significant increase in myocardial oxygen demand in the presence of severe stenosis, revealing physiologically significant ischemia. 1–3 This would be particularly desirable as an alternative to exercise stress testing because some patients are unable to achieve target heart rates due to insufficient motivation, poor physical condition or peripheral vascular disease. Studies with contrast ventriculography using postextrasystolic stimulation and epinephrine infusion have suggested that viable, but poorly contracting myocardium, often responds to these stimuli and can thus be differentiated from infarcted, irreversibly injured myocardium. 4,5 The pharmacologic profile of dobutamine as a relatively selective β-1 agonist 6 suggests that dobutamine also may stimulate viable but “hibernating” myocardium. 5 In this report, the effects of dobutamine infusion on global LV ejection fraction and abnormal LV regional wall motion have been assessed in 15 patients with coronary artery disease. The goal of the study was to determine whether dobutamine “stress” would induce a diminished LV ejection fraction and provoke new LV wall motion abnormalities or improve global and/or regional LV dysfunction.

Pharmacological stress agents for evaluation of ischemic heart disease

Ischemic heart disease is the leading cause of death in the developed countries for those older than 65 years of age. In patients suspected to have coronary artery disease a stress test should be performed to identify the vulnerability of the myocardium to ischemia. As a rule of thumb, the evaluation of coronary artery disease is best done by exercise stress test. In patients who are not able to exercise adequately, pharmacological stress agents are used. The commonly used agents are the coronary vasodilators, adenosine and dipyridamole and the catecholamines, dobutamine and arbutamine. These agents are combined with imaging techniques to increase the sensitivity and specificity of the test. These agents have been widely used and have an excellent safety profile. Another advantage in using pharmacological stress agents is that they do not affect the image quality, especially with echocardiography and magnetic resonance imaging. Ongoing developments hold promise for safer and more reliable pharmacological stress agents in the future.

Effect of Cocaine on Left Ventricular Function Relation to Increased Wall Stress and Persistence After Treatment

BACKGROUND To determine whether alterations in left ventricular (LV) function after a cocaine infusion are due to reduced myocardial contractility or changes in loading conditions, we examined LV function in 30 morphine-sedated, closed-chest dogs. We also wanted to determine the time course of the effects of cocaine on LV function after the infusion was stopped. METHODS AND RESULTS Two-dimensional echocardiography and hemodynamics provided LV fractional shortening and end-systolic wall stress data. Radionuclide ventriculography was also performed. Four groups of dogs received saline or cocaine infusions of 10, 30, or 100 micrograms.kg-1.min-1. Cocaine was infused for 90 minutes with ECG and arterial pressure monitoring. Animals were monitored for an additional 120 minutes after the infusion ended. Arterial pressure rose over the course of the experiment in all four groups, but saline and cocaine 10 micrograms.kg-1.min-1 did not significantly change ejection fraction. Cocaine 30 and 100 micrograms.kg-1.min-1 acutely increased arterial pressure and heart rate but decreased ejection fraction from 0.64 +/- 0.06 to 0.45 +/- 0.08 and from 0.65 +/- 0.10 to 0.46 +/- 0.11, respectively. Additionally, cocaine 100 micrograms.kg-1.min-1 decreased fractional shortening from 36 +/- 9% to 23 +/- 12%. However, cocaine 30 and 100 micrograms.kg-1.min-1 also increased wall stress from 42 +/- 15 to 65 +/- 11 g/cm2 and from 37 +/- 15 to 90 +/- 33 g/cm2, respectively. These results were analyzed by use of the relation between wall stress and fractional shortening as an index of contractility. Fractional shortening after cocaine infusion was displaced downward as a result of increased wall stress rather than changes in contractility. In addition, alteration of afterload with phenylephrine (6 micrograms/kg) and sodium nitroprusside (10 micrograms/kg) before and during infusion of cocaine 100 micrograms.kg-1.min-1 showed similar regression lines for wall stress to fractional shortening. CONCLUSIONS Ejection-phase indexes of LV function were reduced by cocaine in this model of conscious, sedated dogs, but effects were attributable to increased wall stress rather than to reduced myocardial contractility. These effects persisted for at least 2 hours after the infusion was stopped.