Biomedical subjects
Publications and source records attributed to Marc Klapholz.
We report a case of a 56-year-old man with traumatic aortic rupture (TAR) sustained in a motor vehicle accident diagnosed by helical computed tomography, aortography, and transesophageal echocardiography. A large majority of patients with TAR never make it to the hospital, and for those who do, a timely diagnosis is critical for survival. We discuss the merits and pitfalls of the three imaging modalities.
Pericardial constriction secondary to metastatic adenocarcinoma is exceedingly rare. We present the first recorded case of pericardial constriction secondary to metastatic signet-ring mucinous adenocarcinoma diagnosed by echocardiography. The cornerstones of echocardiographic diagnosis of constriction are the following: interventricular septal bounce phasic with respiration, M-mode recordings of the inferior vena cava, and the characteristic Doppler velocity patterns recorded from the mitral valve, hepatic veins, and mitral annulus.
CONTEXT: Nearly 1 million hospitalizations for chronic heart failure occur yearly in the United States, with most related to worsening systemic congestion. Diuretic use, the mainstay therapy for congestion, is associated with electrolyte abnormalities and worsening renal function. In contrast to diuretics, the vasopressin antagonist tolvaptan may increase net volume loss in heart failure without adversely affecting electrolytes and renal function. OBJECTIVE: To evaluate the short- and intermediate-term effects of tolvaptan in patients hospitalized with heart failure. DESIGN, SETTING, AND PARTICIPANTS: Randomized, double-blind, placebo-controlled, parallel-group, dose-ranging, phase 2 trial conducted at 45 centers in the United States and Argentina and enrolling 319 patients with left ventricular ejection fraction of less than 40% and hospitalized for heart failure with persistent signs and symptoms of systemic congestion despite standard therapy. INTERVENTION: After admission, patients were randomized to receive 30, 60, or 90 mg/d of oral tolvaptan or placebo in addition to standard therapy, including diuretics. The study drug was continued for up to 60 days. MAIN OUTCOME MEASURES: In-hospital outcome was change in body weight at 24 hours after randomization; outpatient outcome was worsening heart failure (defined as death, hospitalization, or unscheduled visits for heart failure) at 60 days after randomization. RESULTS: Median (interquartile range) body weight at 24 hours after randomization decreased by -1.80 (-3.85 to -0.50), -2.10 (-3.10 to -0.85), -2.05 (-2.80 to -0.60), and -0.60 (-1.60 to 0.00) kg in the groups receiving tolvaptan 30, 60, and 90 mg/d, and placebo, respectively (P< or =.008 for all tolvaptan groups vs placebo). The decrease in body weight with tolvaptan was not associated with changes in heart rate or blood pressure, nor did it result in hypokalemia or worsening renal function. There were no differences in worsening heart failure at 60 days between the tolvaptan and placebo groups (P =.88 for trend). In post hoc analysis, 60-day mortality was lower in tolvaptan-treated patients with renal dysfunction or severe systemic congestion. CONCLUSION: Tolvaptan administered in addition to standard therapy may hold promise for management of systemic congestion in patients hospitalized for heart failure.
OBJECTIVES: We conducted a prospective multicenter registry in a large metropolitan area to define the clinical characteristics, hospital course, treatment, and factors precipitating decompensation in patients hospitalized for heart failure with a normal ejection fraction (HFNEF). BACKGROUND: The clinical profile of patients hospitalized for HFNEF has been characterized by retrospective analyses of hospital records and state data banks, with few prospective single-center studies. METHODS: Patients hospitalized for heart failure (HF) at 24 medical centers in the New York metropolitan area and found to have a left ventricular (LV) ejection fraction of > or 50% within seven days of admission were included in this registry. Patient demographics, signs and symptoms of HF, coexisting and exacerbating cardiovascular and medical conditions, treatment, laboratory tests, procedures, and hospital outcomes data were collected. Analysis by gender and race was prespecified. RESULTS: Of 619 patients, 73% were women, who were on average four years older than men (72.8 +/- 14.1 years vs. 68.6 +/- 13.8 years, p < 0.001). Black non-Hispanic patients comprised 30% of the study population. They were eight years younger than other patients (66.0 +/- 14.2 years vs. 74 +/- 13.5 years p < 0.001). Co-morbid conditions and their prevalence were: hypertension, 78%; increased LV mass, 82%; diabetes, 46%; and obesity, 46%. Before clinical decompensation that precipitated hospitalization, 86% of patients had chronic symptoms compatible with New York Heart Association functional classes II to IV. Factors precipitating clinical decompensation were identified in 53% of patients. In-hospital mortality was 4.2%. CONCLUSIONS: Patients hospitalized for HFNEF are most often chronically incapacitated elderly women with a history of hypertension and increased LV mass. Reasons for clinical decompensation are identified in only one-half of patients.
We present the case of a patient with severe symptomatic pulmonary hypertension due to rheumatic mitral valve disease who was refractory to traditional therapies, including prostacyclin. Therapy with continuous nesiritide infusion resulted in significant and sustained decreases in pulmonary vascular resistance, an improvement in renal function, and the maintenance of euvolemia.
Cigarette smoking is a major risk factor for the development of coronary artery disease and its complications. Nicotine is one of the major substances that contributes to the pharmacologic activity of cigarette smoke, its toxicity, as well as its addictive nature. Strategies have been developed that utilize nicotine as a replacement substance in motivated patients who wish to stop smoking. Studies have shown that nicotine replacement therapy can be used safely in patients with known coronary artery disease.
Cardiac natriuretic peptides are a family of structurally related peptides that are important in sodium and volume homeostasis. They consist of atrial natriuretic peptide, brain natriuretic peptide, and C-type natriuretic peptide and are elevated in patients with left ventricular dysfunction. In contrast with vasoconstrictive hormones, such as norepinephrine, angiotensin II, and arginine vasopressin, which worsen the physiological milieu in patients with left ventricular dysfunction and heart failure, the natriuretic peptides ameliorate these effects by promoting natriuresis, diuresis, peripheral vasodilation, and by inhibiting the renin-angiotensin system. The serum levels of the natriuretic peptides correlate with the severity of heart failure and appear to have prognostic value. The present article reviews the biochemistry, molecular biology, and physiology of natriuretic peptides and their pathophysiological link to heart failure. The therapeutic uses of natriuretic peptides are also reviewed. This includes the use of intravenous nesiritide, a synthetic human brain natriuretic peptide, and the recently developed vasopeptidase inhibitors which are designed to inhibit the degradation of natriuretic peptides.
The onset of the clinical expression of rheumatic heart disease (RHD) is variable. Exercise or other states that necessitate increased cardiac output often precipitate symptoms. Mitral stenosis (MS) is present in 25% of patients with RHD, and 40% of patients have concomitant MS and mitral regurgitation. About two third of patients with MS have concurrent aortic insufficiency. Pulmonary and tricuspid insufficiency may occur from rheumatic involvement of these valves, or secondary to dilatation of valve annuli from pulmonary hypertension secondary to mitral and/or aortic valve disease. Pregnancy is associated with many hemodynamic changes including expanded intravascular volume, tachycardia, increased intracardiac dimensions, and valvular regurgitation. We report a case of a young female who developed flash pulmonary edema during parturition and was found to have abnormal rheumatic involvement of her aortic, mitral, and tricuspid valves. Successful triple valve repair was performed in a single operation. A review of rheumatic valvular abnormalities, and literature supporting multivalvular repair for rheumatic heart disease is provided.