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Biomedical subjects

Kanu Chatterjee

Publications and source records attributed to Kanu Chatterjee.

At least 19 recordsLinked to original sources
PubMed2007

The utility of gestures in patients with chest discomfort.

PURPOSE: Patient gestures are thought to be useful in determining the etiology of chest discomfort. We sought to determine the utility of certain patient gestures in the diagnosis of ischemic chest discomfort or myocardial infarction. METHODS: We performed a prospective observational study of 202 patients admitted with chest discomfort. Patients were observed for the Levine Sign (clenched fist to the chest), the Palm Sign (palm of the hand to the chest), the Arm Sign (touching the left arm), and, as an indicator of nonischemic chest discomfort, the Pointing Sign (pointing with 1 finger). RESULTS: Prevalences of the Levine, Palm, Arm, and Pointing Signs were 11%, 35%, 16%, and 4%, respectively. Using troponin levels and results of functional studies and coronary angiograms as reference standards, none of the sensitivities of the signs exceeded 38%. Specificities of the Levine and Arm Signs ranged between 78% and 86%, but the positive predictive values did not exceed 55%. The Pointing Sign had a specificity of 98% for evidence of nonischemic chest discomfort, and the positive predictive value of a negative troponin was 88%. The diameter of discomfort significantly correlated with certain gestures. Larger chest pain diameters were associated with evidence of myocardial ischemia. CONCLUSIONS: Although certain gestures are exhibited by patients presenting with chest discomfort, they generally have poor test characteristics. The Pointing Sign has a high specificity for nonischemic chest discomfort, but a low prevalence. The gestures may communicate the size of the chest discomfort, with larger areas suggestive of ischemia.

Biomarkers↗
PubMed2006

ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing Committee to Revise the 1998 guidelines for the management of patients with valvular heart disease) developed in collaboration with the Society of Cardiovascular Anesthesiologists endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons.

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Heart Valve Diseases↗
PubMed2006

Relationship between accurate auscultation of a clinically useful third heart sound and level of experience.

BACKGROUND: Poor performance by physicians-in-training and interobserver variability between physicians have diminished clinicians' confidence in the value of the third heart sound (S3). METHODS: To determine whether auscultation of a clinically useful S3 improves with advancing levels of experience, we performed a prospective, blinded, observational study of 100 patients undergoing left-sided heart catheterization. Patients underwent blinded auscultation by 4 physicians (each from 1 of 4 different levels of experience), phonocardiography, measurement of blood B-type natriuretic peptide levels, echocardiography for measurement of left ventricular ejection fraction, and cardiac catheterization for measurement of left ventricular end-diastolic pressure. RESULTS: Whereas residents' and interns' auscultatory findings demonstrated no significant agreement with phonocardiographic findings, an S3 auscultated by cardiology fellows (kappa = 0.37; P<.001) and cardiology attendings (kappa = 0.29; P = .003) agreed with phonocardiographic findings. Although the sensitivities of the S3 were low (13%-52%) for identifying patients with abnormal measures of left ventricular function, the specificities were high (85%-95%), with the best test characteristics exhibited by phonocardiography and more experienced physicians. The S3 detected by attendings and fellows was superior in distinguishing an elevated B-type natriuretic peptide level, a depressed left ventricular ejection fraction, or an elevated left ventricular end-diastolic pressure (P = .002-.02 for attendings and .02-.03 for fellows) compared with residents (P = .02-.47) or interns (P = .09-.64). CONCLUSIONS: The S3 auscultated by more experienced physicians demonstrated fair agreement with phonocardiographic findings. Although correlations were superior for phonocardiography, the associations between the S3 and abnormal markers of left ventricular function improved with each level of auscultator experience.

Adult↗
PubMed2006

High-sensitivity C-reactive protein and parameters of left ventricular dysfunction.

BACKGROUND: Elevated levels of high-sensitivity C-reactive protein (CRP), an inflammatory marker, have been associated with heart failure. However, it is not known which parameters of left ventricular dysfunction correlate with elevated levels of CRP. METHODS AND RESULTS: In this cross-sectional study of 98 patients referred for cardiac catheterization, we investigated whether commonly used clinical indices of left ventricular dysfunction correlated with CRP levels. CRP levels were elevated to a greater degree in participants with diabetes mellitus (P =.006) and heart failure (P =.003). Increased CRP levels were associated with increased plasma levels of B-type natriuretic peptide (BNP; P =.0001), decreased left ventricular ejection fraction (LVEF; P =.02), and increased left-ventricular end-diastolic pressure (LVEDP; P =.0005). After multivariable adjustment, LVEDP and CRP were independently associated (P =.046). CONCLUSION: CRP is increased in patients with heart failure. Of the clinical parameters of left ventricular dysfunction, direct measurement of left ventricular end-diastolic pressure is most closely associated with CRP.

Aged↗
PubMed2006

Nesiritide acutely increases pulmonary and systemic levels of nitric oxide in patients with pulmonary hypertension.

BACKGROUND: Pulmonary hypertension (PH) is characterized by decreased pulmonary vascular expression of nitric oxide (NOx), a vasodilator that increases levels of smooth muscle cyclic guanosine monophosphate (cGMP). This study investigated mechanisms by which the vasodilator B-type natriuretic peptide (BNP) affects the systemic and pulmonary vasculature in PH patients. METHODS AND RESULTS: Twenty PH patients with mean pulmonary artery (PA) pressure > 25 mm Hg were enrolled. Ten had precapillary (pulmonary capillary wedge pressure [PCWP] < or = 15 mm Hg) and 10 had postcapillary (PCWP > 15 mm Hg) PH. Right heart catheterization was performed before and 30 minutes after intravenous nesiritide infusion. NOx and cGMP levels from the PA and systemic (AO) arteries were obtained before and after nesiritide infusion. The postcapillary PH patients demonstrated significantly reduced pulmonary vascular resistance after nesiritide; there was no change in the precapillary PH cohort. NOx levels increased significantly in both AO (P < .0001) and PA (P = .0093), as did cGMP levels (P < .0001). There was a higher increase in NOx levels from the pulmonary arteries in precapillary PH patients compared to postcapillary PH patients (P = .020). CONCLUSION: In PH patients, nesiritide infusion significantly increases NOx levels, suggesting a novel mechanism for its vasodilatory effects. These responses may differ between pre- and postcapillary PH patients.

Adult↗
PubMed2005

Association between phonocardiographic third and fourth heart sounds and objective measures of left ventricular function.

CONTEXT: The third (S3) and fourth (S4) heart sounds detected by phonocardiography are considered to represent the criterion standards of the gallop sounds, but their test characteristics have not been explored. OBJECTIVE: To determine the diagnostic test characteristics of the S3 and S4 for prediction of left ventricular dysfunction using a computerized heart sound detection algorithm. DESIGN, SETTING, AND PARTICIPANTS: Prospective study of 90 adult patients undergoing elective left-sided heart catheterization at a single US teaching hospital between August 2003 and June 2004. The mean age was 62 (SD, 13) years (range, 24-90 years) and 61 (68%) were male. Within a 4-hour period, participants underwent computerized heart sound phonocardiographic analysis, cardiac catheterization, transthoracic echocardiography, and blood sampling for assessment of an S3/S4, left ventricular end-diastolic pressure (LVEDP), left ventricular ejection fraction (LVEF), and B-type natriuretic peptide (BNP), respectively. MAIN OUTCOME MEASURES: Diagnostic test characteristics of the computerized phonocardiographic S3 and S4 using markers of left ventricular function as criterion standards. RESULTS: Mean (SD) LVEDP was significantly elevated (18.4 [6.9] mm Hg vs 12.1 [7.3] mm Hg; P<.001), mean (SD) LVEF was reduced (49.4% [20.2%] vs 63.6% [14.8%]; P<.001), and median (interquartile range) BNP was elevated (330 [98-1155] pg/mL vs 86 [41-192] pg/mL; P<.001) in those with an S3, S4, or both compared with patients without a diastolic heart sound. The sensitivities of these heart sounds to detect an elevated LVEDP, reduced LVEF, or elevated BNP were 41%, 52%, and 32% for an S3, and 46%, 43%, and 40% for an S4, respectively. For abnormal levels of the same markers of ventricular function, the specificities of the S3 were 92%, 87%, and 92%, while the specificities of the S4 were 80%, 72%, and 78%, respectively. CONCLUSIONS: Neither the phonocardiographic S3 nor the S4 is a sensitive marker of left ventricular dysfunction. The phonocardiographic S3 is specific for left ventricular dysfunction and appears to be superior to the moderate specificity of the phonocardiographic S4.

Adult↗
PubMed2005

Neurohormonal activation in congestive heart failure and the role of vasopressin.

Vasoactive neurohormonal systems (eg, sympathetic nervous system [SNS], renin-angiotensin-aldosterone system, and arginine vasopressin [AVP]) are defense mechanisms designed to preserve arterial volume and circulatory homeostasis during periods of low cardiac output. Neurohormonal systems, which are normally stimulated under conditions of acute volume depletion, are activated by the low cardiac output and arterial pressure. However, sustained and chronic activation of these systems, as occurs in congestive heart failure (CHF), can cause progressive ventricular remodeling and worsening heart failure. Vasoconstriction, water retention, and increased blood volume are results of the activation of the SNS, the renin-angiotensin pathway, and AVP secretion. These effects can accelerate progression of CHF, contributing to increased morbidity and mortality. AVP regulates vascular tone and free-water reabsorption, respectively, through the vasopressin V(1a) and V(2) receptor subtypes and therefore is a potential neurohormonal target in the treatment of CHF.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2005

Effects of intravenous levosimendan on human coronary vasomotor regulation, left ventricular wall stress, and myocardial oxygen uptake.

BACKGROUND: Levosimendan is a calcium-sensitizing agent and an inodilator under current investigation in the treatment of decompensated heart failure. The effects of intravenous levosimendan on the human coronary vasculature, together with myocardial wall stress and oxygen uptake, have not been adequately studied. METHODS AND RESULTS: Ten adult patients underwent right- and left-heart catheterization. Baseline coronary blood flow was determined with quantitative coronary angiography and an intracoronary Doppler-tipped guidewire. Myocardial oxygen uptake was measured with a coronary sinus catheter. Echocardiography was performed before and 30 minutes after an intravenous infusion of levosimendan (24-microg/kg bolus over 10 minutes) was begun. Pulmonary capillary wedge decreased 37% (P=0.009), cardiac output increased 9% (P=0.04), and systemic vascular resistance decreased 18% (P<0.001). Left ventricular ejection fraction increased 20% (P=0.009), and meridional systolic wall stress decreased 48% (P=0.009). Coronary artery diameter increased 10% at 15 minutes (P=0.001) and 11% at 30 minutes (P=0.01). Coronary artery velocity increased 10% over baseline (P=0.04). Coronary blood flow increased 45% (P=0.02), whereas coronary resistance decreased 36% at 30 minutes (P=0.03). Myocardial oxygen extraction decreased 9% at 30 minutes (P=0.04). CONCLUSIONS: Levosimendan given intravenously exerts vasodilator effects on human coronary conductance and resistance arteries. Despite a decrease in coronary perfusion pressure, coronary blood flow is increased. A reduction in coronary vascular resistance and a decrease in coronary venous oxygen content indicate primary coronary vasodilation by levosimendan. Improved left ventricular systolic function and decreased myocardial oxygen extraction suggest improved myocardial efficiency.

Adult↗
PubMed2005

Effects of intravenous nesiritide on pulmonary vascular hemodynamics in pulmonary hypertension.

BACKGROUND: Nesiritide is effective in the treatment of decompensated heart failure (HF). We evaluated the acute hemodynamic effects of nesiritide, a recombinant B-type natriuretic peptide, in patients with HF and pulmonary hypertension (PH). METHODS AND RESULTS: Twenty patients with HF and PH (mean pulmonary arterial [PA] pressure >25 mm Hg) were enrolled: 10 with postpulmonary capillary wedge (PCW) >15 mm Hg and 10 with precapillary PH (PCW) < or =15. The pulmonary and systemic hemodynamics were determined by right heart catheterization at baseline and at 15 and 30 minutes after an intravenous nesiritide infusion (2 mcg/kg bolus and 0.01 mcg.kg.min). For the patients with postcapillary PH, the mean left ventricular ejection fraction was 28 +/- 15%. After the 30-minute nesiritide infusion, right atrial (RA) pressure decreased 48% (P < .0001), mean PA pressure decreased 29% (P < .0001), PCW pressure decreased 40% (P < .0001), cardiac index (CI) increased 35% (P = .009), pulmonary vascular resistance index (PVRI) decreased 35% (P = .01), and arteriovenous oxygen difference (AVDO(2)) decreased 27% (P = .0003). For precapillary PH patients, there was no change in RA, PA, or PCW pressure, nor any change in CI, PVRI, or AVDO(2). CONCLUSIONS: Nesiritide acutely and significantly reduced PA pressure, PVRI, and biventricular filling pressures in patients with postcapillary PH. However, for patients with precapillary PH, nesiritide had no significant acute hemodynamic effect on the pulmonary hemodynamics. The lack of acute beneficial effects of nesiritide in patients with advanced precapillary PH may be related to their relatively fixed remodeling of the pulmonary vasculature.

Adult↗
PubMed2005

Dehydroepiandrosterone sulfate induces acute vasodilation of porcine coronary arteries in vitro and in vivo.

Although an inverse relationship between dehydroepiandrosterone sulfate (DHEAS) and coronary artery disease has been demonstrated in men, the vascular effects of DHEAS are not well defined. The vasoactive effects of intracoronary DHEAS and testosterone (0.1 nM to 1 microM) were examined in vivo in 24 pigs. Epicardial cross-sectional area was measured by intravascular ultrasound, and coronary flow velocity by intravascular Doppler velocimetry. We also examined the effects of antagonism of the androgen receptor, nitric oxide synthase, and potassium channels on DHEAS-induced vasodilation in vitro in coronary rings from male and female pig hearts. DHEAS and testosterone induced increases in cross-sectional area, average peak velocity, and coronary blood flow. The maximal increase in coronary blood flow in response to testosterone was 1.26-fold (P=0.02), and in average peak velocity 1.43-fold (P=0.05), greater than that to DHEAS, whereas increases in cross-sectional area were similar. Vasodilation to both hormones was rapid, with maximal responses occurring <10 minutes after administration. In vitro, DHEAS and testosterone induced vasodilation in coronary rings, greater with testosterone. At doses of 0.1 and 1 microM, the vasodilator effects of DHEAS and testosterone were inhibited by the androgen receptor antagonist flutamide but not the estrogen receptor antagonist ICI 182,780. At 10 microM, neither DHEAS- nor testosterone-induced vasorelaxation was inhibited by flutamide, ICI 182,780, L-NAME, or deendothelialization, but both were attenuated by pretreatment with glibenclamide. No gender differences were observed in any of the responses examined. In conclusion, DHEAS is an acute coronary artery vasodilator, but less potent than testosterone. Its effect might be mediated via androgen receptors and may involve ATP-sensitive potassium channels.

ATP-Binding Cassette Transporters↗
PubMed2003

Effects of intravenous nesiritide on human coronary vasomotor regulation and myocardial oxygen uptake.

BACKGROUND: Nesiritide, recombinant human B-type natriuretic peptide, has been shown to be efficacious in the treatment of decompensated heart failure. The effects of intravenous nesiritide on the human coronary vasculature have not been studied. METHODS AND RESULTS: Ten patients underwent right and left heart catheterization. Baseline coronary blood flow was determined using quantitative coronary angiography (QCA) and an intracoronary Doppler-tipped guidewire. Myocardial oxygen uptake was measured using a coronary sinus catheter. Patients then received an intravenous infusion of nesiritide (2 microg/kg bolus followed by 0.01 microg/kg per min infusion) for 30 minutes. Right atrial pressure decreased 52% (P=0.012), pulmonary artery mean pressure decreased 19% (P=0.03), pulmonary capillary wedge pressure decreased 46% (P=0.002), and mean arterial pressure decreased 11% (P=0.007). QCA demonstrated a 15% increase in coronary artery diameter from a baseline of 2.6+/-0.8 to 3.0+/-0.8 mm at 30 minutes (P=0.007). The coronary velocity measure of average peak velocity increased 14% from 20.8+/-6.4 at baseline to 23.8+/-7.2 cm/s at 5 minutes (P=0.015) and then returned to baseline for the remainder of the infusion. Coronary blood flow increased 35% (P=0.007), whereas coronary resistance decreased 23% at 15 and 30 minutes (P=0.036). Myocardial oxygen uptake decreased 8% during the nesiritide infusion (P=0.043). CONCLUSIONS: Nesiritide exerts coronary vasodilator effects on both the coronary conductance and resistance arteries. Despite a decrease in coronary perfusion pressure, coronary artery blood flow is increased, coronary resistance is decreased, and myocardial oxygen uptake is decreased.

Adult↗