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Biomedical subjects

Kanu Chatterjee

Publications and source records attributed to Kanu Chatterjee.

31 records · Page 2Linked to original sources
PubMed2003

Role of nonglycosidic inotropic agents: indications, ethics, and limitations.

Nonglycosidic inotropic agents have been used for the short-term management of low output states and hypotension complicating acute myocardial infarction for several years. Without adequate reperfusion of the ischemic myocardium, inotropic agents are seldom effective in producing sustained hemodynamic responses. Furthermore, the potential exists for enhancement of ischemia and extension of myocardial necrosis. Thus, inotropic and vasopressors therapy should be regarded as temporary supportive treatment in patients with acute coronary syndrome and should be discontinued as soon as feasible. Parenteral sympathomimetic agents, usually dobutamine, and phosphodiesterase inhibitors, usually milrinone, are used for the management of exacerbations of chronic systolic heart failure. Although hemodynamics, and occasionally clinical status, improve, such therapy is associated with increased mortality and can potentially hasten a patient's demise. Nonparenteral sympathomimetics, such as ibopamine, phosphodiesterase-III inhibitors, such as milrinone and enoximone, calcium-sensitizing agents, such as pimobendan, and other novel inotropic agents, such as vesnarinone, all increase mortality of patients with chronic heart failure. Furthermore, newer noninotropic agents, such as B-natriuretic peptide, have been introduced for treatment of decompensated heart failure. New nonpharmacologic devices, such as biventricular pacing, are available for the treatment of advanced heart failure. Thus, indications for the use of presently available nonglycosidic inotropic agents are limited and should be considered only for short-term therapy or when no other treatment is available.

Adrenergic beta-Antagonists↗
PubMed2003

Amiodarone rescue therapy for severe decompensated heart failure initially unsuitable for beta-blockers.

BACKGROUND: Beta-blocker therapy is now standard therapy for patients with stable heart failure; however, fluid-overloaded, New York Heart Association Class IV patients tolerate beta-blockers poorly. Amiodarone, a drug with antiadrenergic effects, has been shown to improve survival for patients with heart rates of 90 beats per minute or greater. METHODS: We reviewed 26 patients with severe decompensated heart failure who were started on oral amiodarone for heart rate control. beta-Blocker titration was attempted when patients became clinically stable. RESULTS: The mean age of the patients was 48.5 +/- 17.5 years, and 73% were male. Fifteen patients were New York Heart Association Class IV, and 11 were Class III. Of these, 23 (88%) were fluid-overloaded, and 11 (42%) were on inotropic agents when amiodarone was started. The mean ejection fraction was 16.1 +/- 6%. The initial dose of amiodarone was 346 +/- 120 mg/day. Twenty (77%) patients were successfully started on beta-blockers. At follow-up prior to beta-blockers, 20 (77%) patients improved by at least one New York Heart Association class. Heart rate decreased from a mean of 98 +/- 15 to 78 +/- 13 beats per minute (P <.0001). Echocardiograms were available in 12 patients, with ejection fractions increasing from 16.1 +/- 8% to 26.8 +/- 13% (P =.004). CONCLUSIONS: Amiodarone may be an effective rescue therapy for patients with decompensated heart failure and serve as a bridge to subsequent beta-blocker therapy.

Adrenergic beta-Antagonists↗
PubMed2003

Comparative effects of aspirin with ACE inhibitor or angiotensin receptor blocker on myocardial infarction and vascular function.

OBJECTIVES: We previously showed that an angiotensin-converting enzyme inhibitor (captopril) or an angiotensin receptor blocker (losartan) reduced infarct size and improved endothelial function in a rat model of ischaemia-reperfusion. The present study was undertaken to see if aspirin (ASA) antagonised the beneficial effects of captopril or losartan. METHODS: One hundred and fourteen Sprague-Dawley rats were randomised into six groups; Control, ASA, captopril, losartan, ASA+captopril, and ASA+losartan. ASA, captopril or losartan were given at a concentration of 40 mg/kg/day in drinking water. After six weeks of pre-treatment, the rats were subjected to 17 minutes of left anterior descending coronary artery occlusion and 120 minutes of reperfusion, with haemodynamic and ECG monitoring. During the reperfusion period, the effective refractory period (ERP), ventricular fibrillation threshold (VFT) and bleeding time (BT) were measured. In fresh aortic rings precontracted with phenylephrine, endothelium-dependent and -independent relaxations were assessed using acetylcholine and nitroglycerin. RESULTS: Haemodynamic changes were not different between the groups. Serum ASA concentrations were 0.5, 1.1 and 0.6 mg/dl in the ASA, ASA+captopril and ASA+losartan groups, respectively, and BT was prolonged (p<0.01). ASA alone reduced endothelium-dependent relaxation (-29+8 vs. -69+11%, p<0.01), but did not change endothelium-independent relaxation. ASA did not affect endothelial relaxation induced by acetylcholine in the presence of either captopril or losartan. Angiotensin I and ERP were elevated by captopril and losartan. Angiotensin II and VFT were elevated by losartan. ASA with captopril, captopril and losartan equally reduced infarct size, compared with control (39+3, 39+4, and 39+5 vs. 53+3%, all p<0.05). CONCLUSIONS: Captopril and losartan had similar cardiovascular protective effects in a rat model of ischaemia-reperfusion. Aspirin did not attenuate the cardiovascular protective effects of captopril or losartan.

Angiotensin I↗
PubMed2003

Constrictive pericarditis and restrictive cardiomyopathy: similarities and differences.

Constrictive pericarditis and restrictive cardiomyopathy, two relatively uncommon clinical conditions, create a diagnostic dilemma primarily because of the many similarities in both their clinical and hemodynamic presentations. However, considerable differences exist in the pathophysiology, management, and prognosis between these two syndromes. Furthermore, the precise diagnosis of constrictive pericarditis and restrictive cardiomyopathy is mandatory, as the former is often curable whereas only palliative treatments are available for the latter. In this brief review, similarities and differences in the various aspects of constrictive pericarditis and restrictive cardiomyopathy will be discussed.

Cardiomyopathy, Restrictive↗
PubMed2002

Pulmonary hypertension: hemodynamic diagnosis and management.

Hemodynamic classification of pulmonary hypertension relates to the hemodynamic mechanisms of pulmonary arterial hypertension, such as abnormalities of pulmonary blood flow, pulmonary vascular resistance, and pulmonary venous pressures. The therapeutic approaches can be directed to the hemodynamic mechanisms of pulmonary hypertension.

Hemodynamics↗
PubMed2002

Effects of long-term biventricular stimulation for resynchronization on echocardiographic measures of remodeling.

BACKGROUND: Long-term ventricular resynchronization therapy improves symptom status. Changes in left ventricular remodeling have not been adequately evaluated. METHODS AND RESULTS: Fifty-three patients with systolic heart failure and bundle-branch block underwent implantation of biventricular stimulation (BVS) devices as part of a randomized trial. Echocardiograms were acquired at randomization and at 6-week intervals until completion of 12 weeks of continuous BVS. There were no changes in heart rate or QRS duration after 12 weeks of BVS. Serum norepinephrine values did not change with BVS. After 12 weeks of BVS, left atrial volume decreased. Left ventricular end-systolic and end-diastolic dimensions and left ventricular end-systolic volume also decreased after 12 weeks of BVS. Sphericity index did not change. Measures of systolic function, including left ventricular outflow tract and aortic velocity time integral and myocardial performance index, improved. CONCLUSIONS: Long-term resynchronization therapy results in atrial and ventricular reverse remodeling and improved hemodynamics.

Adult↗
PubMed2002

Congestive heart failure: what should be the initial therapy and why?

Left ventricular systolic dysfunction is associated with neurohormonal activation which contributes to progressive ventricular remodeling and worsening clinical heart failure. Renin-angiotensin-aldosterone and sympathetic nervous systems are activated, not only in patients with clinically overt heart failure, but also in patients with asymptomatic or minimally symptomatic left ventricular systolic dysfunction. Activation of the angiotensin and adrenergic systems produces deleterious effects on systemic and coronary hemodynamics, promotes myocyte hypertrophy and fibroblast growth, and myocyte necrosis and apoptosis. Thus, therapy of heart failure should consist of pharmacologic agents not only to relieve symptoms but also to prevent and attenuate ventricular remodeling and progressive heart failure, thereby improving prognosis. In patients who are symptomatic, ACE inhibitors along with digitalis and diuretics as initial therapy (triple therapy) have the greater potential to improve exercise tolerance and decrease the incidence of treatment failure compared with diuretics alone or a combination of diuretics and digitalis. Diuretics alone should not be considered for long-term therapy as plasma renin activity, angiotensin II, aldosterone, norepinephrine and vasopressin levels may increase. ACE inhibitors decrease mortality in patients with heart failure resulting from left ventricular systolic dysfunction. The results of presently available studies indicate that angiotensin II receptor blockers (ARBs) do not provide any advantage over ACE inhibitors regarding survival benefit but may be better tolerated. Long-term adrenergic inhibition with the use of ss-adrenoceptor antagonists added to ACE inhibitors is associated with attenuation of ventricular remodeling, improvement in ventricular function and clinical class and survival of patients with symptomatic systolic left ventricular failure. Thus, initial pharmacotherapy for systolic heart failure should consist of: maximal tolerated dosages of ACE inhibitors;ARBs if ACE inhibitors are not tolerated because of intractable cough or angioedema;adequate dosages of hydralazine and isosorbide dinitrate if ACE inhibitors or ARBs are not tolerated; relatively low dosages of digoxin (serum concentrations of < or = 1.0 ng/dl) if not contraindicated; and diuretics to relieve congestive symptoms. Addition of spironolactone to ACE inhibitors can result in a significant reduction in the risk of sudden death in patients with symptomatic severe heart failure. Myocardial infarction resulting from ischemic heart disease is the most common cause of systolic left ventricular failure and the therapeutic modalities with potential to reduce the risks of myocardial infraction, such as risk factor modification, adequate control of diabetes and hypertension, antiplatelet agents and lipid-lowering agents, should also be included in the initial therapy.

Adrenergic Antagonists↗
PubMed2002

The renin-angiotensin system does not contribute to the endothelial dysfunction and increased infarct size in rats exposed to second hand smoke.

INTRODUCTION: Both second hand smoke (SHS) and the renin-angiotensin system (RAS) contribute to endothelial dysfunction and increased infarct size in a rat ischaemia-reperfusion model. However, the potential interaction between SHS and the RAS is unknown. METHODS: Eighty-four rats were randomised into four groups: group C was a normal control; L was given 40 mg/kg/day of losartan in drinking water; SC and SL were exposed to SHS (smoking chamber) and given regular water or 40 mg/kg/day of losartan in drinking water, respectively. After six weeks of pre-treatment, rats were subjected to 17 minutes of left coronary artery occlusion and 2 hours of reperfusion with haemodynamic and ECG monitoring. RESULTS: Haemodynamics were not significantly different among the four groups. Losartan increased the threshold for ventricular fibrillation (p=0.0001) and reduced spontaneous ventricular arrhythmias (p=0.002) during ischaemia-reperfusion, while SHS did not (p=0.713, 0.110), and there was no interaction between losartan and SHS. The maximal endothelium-dependent vasorelaxation induced by a calcium ionophore (A23187) was increased by losartan (p=0.007). Myocardial infarct size was smaller in the losartan groups (p=0.032), larger in the SHS groups (p=0.0001), and there was no significant interaction. CONCLUSION: In conclusion, losartan decreased infarct size and increased endothelium-dependent vasorelaxation. SHS exposure impaired endothelial function and increased infarct size. The effects of losartan and SHS were consistently independent of each other. These results suggest that the RAS does not contribute to the adverse effects of SHS.

Angiotensin II↗
PubMedDate not supplied

Primary diastolic heart failure.

Diastolic heart failure is defined clinically when signs and symptoms of heart failure are present in the presence of preserved left ventricular systolic function (ejection fraction >45%). The incidence and prevalence of primary diastolic heart failure increases with age and it may be as high as 50% in the elderly. Age, female gender, hypertension, coronary artery disease, diabetes, and increased body mass index are risk factors for diastolic heart failure. Hemodynamic consequences such as increased pulmonary venous pressure, post-capillary pulmonary hypertension, and secondary right heart failure as well as decreased cardiac output are similar to those of systolic left ventricular failure, although the nature of primary left ventricular dysfunction is different. Diagnosis of primary diastolic heart failure depends on the presence of preserved left ventricular ejection fraction. Assessment of diastolic dysfunction is preferable but not mandatory. It is to be noted that increased levels of B-type natriuretic peptide does not distinguish between diastolic and systolic heart failure. Echocardiographic studies are recommended to exclude hypertrophic cardiomyopathy, infiltrative heart disease, primary valvular heart disease, and constrictive pericarditis. Myocardial stress imaging is frequently required to exclude ischemic heart disease. The prognosis of diastolic heart failure is variable; it is related to age, severity of heart failure, and associated comorbid diseases such as coronary artery disease. The prognosis of severe diastolic heart failure is similar to that of systolic heart failure. However, cautious use of diuretics and/or nitrates may cause hypotension and low output state. Heart rate control is essential to improving ventricular filling. Pharmacologic agents such as angiotensin receptor blockers, angiotensin-converting enzyme inhibitors, and calcium channel blockers are used in selected patients to decrease left ventricular hypertrophy. To decrease myocardial fibrosis, aldosterone antagonists have a potential therapeutic role. However, prospective controlled studies will be required to establish their efficacy in primary diastolic heart failure.

Aged↗
PubMedDate not supplied

Obese patients have lower B-type and atrial natriuretic peptide levels compared with nonobese.

Obesity is a risk factor for the development of heart failure, but the causal mechanism remains unclear. Impaired production or enhanced clearance of natriuretic peptides, which regulate sodium balance and sympathetic activation, may play an important role. The authors investigated the relationship of plasma B-type natriuretic peptide and atrial natriuretic peptide levels to body mass index in 100 patients referred for left heart catheterization. Hemodynamic and echocardiographic data were obtained for all study participants. Atrial natriuretic peptide and B-type natriuretic peptide levels were compared in obese (body mass index > or = 30 kg/m2) and nonobese (body mass index < 30 kg/m2) subjects. Multivariate regression analyses were performed, adjusting for clinical and hemodynamic covariates. Obese patients had significantly lower B-type natriuretic peptide (p = 0.03) and atrial natriuretic peptide (p = 0.04) levels compared with nonobese. Multivariate analysis revealed lower B-type natriuretic peptide (p = 0.095) and atrial natriuretic peptide (p = 0.007) levels in obese patients while controlling for age, sex, left ventricular end-diastolic pressure, and left ventricular ejection fraction. Low levels of circulating natriuretic peptides are thus associated with obesity and may contribute to the development of heart failure.

Atrial Natriuretic Factor↗