John P. Girod

Plasma B-Type Natriuretic Peptide Levels in Ambulatory Patients With Established Chronic Symptomatic Systolic Heart Failure

Background—The diagnostic and prognostic values of plasma B-type natriuretic peptide (BNP) testing are established. However, the range of plasma BNP levels present in the setting of chronic, stable systolic heart failure (HF) is unclear. Methods and Results—We followed up 558 consecutive ambulatory patients with chronic, stable systolic HF (left ventricular ejection fraction <50%) treated at a specialized outpatient HF clinic between November 2001 and February 2003. Retrospective chart review was performed to determine clinical and functional data at the time of BNP testing (Biosite Triage). The clinical characteristics of patients with plasma BNP levels <100 pg/mL and those with ≥100 pg/mL were compared. In our cohort, 60 patients were considered asymptomatic, and their plasma BNP levels ranged from 5 to 572 pg/mL (median, 147 pg/mL). Of the remaining 498 symptomatic (NYHA functional class II–III) patients, 106 (21.3%) had plasma BNP levels in the “normal” diagnostic range (<100 pg/mL). Patients in this “normal BNP” subgroup were more likely to be younger, to be female, to have nonischemic pathogenesis, and to have better-preserved cardiac and renal function and less likely to have atrial fibrillation. Conclusions—In the ambulatory care setting, both symptomatic and asymptomatic patients with chronic, stable systolic HF may present with a wide range of plasma BNP levels. In a subset of symptomatic patients (up to 21% in our cohort), plasma BNP levels are below what would be considered “diagnostic” (<100 pg/mL).

Tako-Tsubo–Like Transient Left Ventricular Dysfunction

A 68-year-old woman presented with mild chest pressure typical of myocardial ischemia. The initial ECG revealed normal sinus rhythm with ST-segment elevations in leads V2 through V5 (Figure 1). Troponin T level was 3.4 ng/mL (normal <0.01 ng/mL), and creatinine kinase level was 250 U/L (normal <220 U/L). The patient underwent emergency coronary angiography, which demonstrated minimal atherosclerotic disease. However, contrast left ventriculography demonstrated marked akinesis of the mid …

Can Glucocorticoid Homeostasis Explain the Antiatherogenic Effect of Peripheral Adiposity

To the Editor: Tanko et al1 observed that peripheral adiposity in elderly women may be associated with a relatively reduced risk of insulin resistance, dyslipidemia, and vascular calcification. They suggested that this benefit reflects an antiatherogenic effect of peripheral fat. However, we believe their findings support the concept that subtly increased glucocorticoid activity may exert dysmetabolic and atherogenic effects. It is well known, for example, that supraphysiologic levels of glucocorticoids, as seen in Cushing syndrome, increase central adiposity at the expense of peripheral adiposity and muscle mass. In recent years, there has been increasing evidence that connects physiologically elevated endogenous glucocorticoid activity with visceral obesity—a phenomenon that may be mediated at the central level …

The metabolic syndrome as a vicious cycle: does obesity beget obesity?

Most attempts at weight loss are frustrated by the bodys propensity to maintain fat mass. There are genetic and environmental mechanisms behind this phenomenon, such as thrifty genes, sedentary lifestyle and abundant food resources. We will outline a physiologic mechanism that may perpetuate obesity once it develops. Specifically, we suggest that obesity-induced hyperinsulinemia facilitates fuel storage as fat. This can be exacerbated by high glucocorticoid activity, low growth hormone (GH) activity and the paradoxical increase in free fatty acid (FFA) flux resulting from basal lipolysis in an expanded fat mass. We also outline mechanisms by which obesity may perpetuate low GH and increased glucocorticoid activity in the metabolic syndrome.

Moricizine Induced Increase in Pacing Threshold

GIROD, J.P., et al.: Moricizine Induced Increase in Pacing Threshold. A 72‐year‐old woman who was experiencing incessant ventricular tachycardia and recurrent automatic implantable cardioverter defibrillator (AICD) firing despite amiodarone therapy was referred to the Cleveland Clinic Foundation. Myocardial ischemia and infarction were ruled out by standard means. Several antiarrhythmic medications were tried previously without success. Moricizine, 200 mg three times daily, was initiated and controlled the ventricular tachycardia. However, after the dose of moricizine was titrated upward, the patient became symptomatically bradycardic and the ECG exhibited 2:1 block of her paced rhythm and an increased ventricular pacing threshold. (PACE 2003; 26[Pt. I]:110–111)

Does glucocorticoid dysregulation contribute to the link between cigarette smoking and insulin resistance

In a recent issue of the Journal , Drs. Reaven and Tsao [(1)][1]discussed the association between cigarette smoking and insulin resistance, endothelial dysfunction, and dyslipidemia. They assert that insulin resistance may be a key mechanism by which smoking increases the risk of atherosclerotic

Postmenopausal Hormones and Glycemic Effects

TO THE EDITOR: We read with interest Kanaya and colleagues’ report that combination hormone replacement therapy (HRT) reduced the incidence of type 2 diabetes mellitus by 35% (6.2% vs. 9.5% [P 0.006]; number needed to treat for benefit [NNTB] for 4 years 30) among postmenopausal women with coronary disease (1). We wonder whether the authors can comment on the possible contribution of exercise to the observed effect. Kanaya and colleagues analyzed several potential mediators of treatment effect on diabetes incidence, including waist circumference, body mass index (BMI), change in weight, smoking, markers of the metabolic syndrome, and certain cardiac medications, but they did not mention exercise. In the Diabetes Prevention Program, a randomized, controlled trial (2), a lifestyle intervention designed to achieve goals of a 7% reduction in body weight and 150 minutes of physical activity per week was more effective than metformin or placebo in preventing diabetes (NNTB for 3 years 7). The remarkable effect of the lifestyle intervention observed in the Diabetes Prevention Program and the fact that Kanaya and colleagues reported baseline levels of physical activity make us wonder whether Kanaya and colleagues have follow-up data regarding physical activity. As the authors noted, the mechanism by which combination HRT might prevent diabetes is unknown. Is it possible that a change in exercise amount in persons taking estrogen compared with controls could explain the results?