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Survival outcomes of patients with heart failure (HF) based on their disease etiology are not well described. Here, we provide one-year mortality outcomes of 10850 patients with HF (mean age = 59.9 years, 31% women) in India. Ischemic heart disease (71.9%), dilated cardiomyopathy (17.3), rheumatic heart disease (5.4), non-rheumatic valvular heart disease (1.9), hypertrophic cardiomyopathy (0.8), congenital heart disease (0.7), peri-partum cardiomyopathy (0.5), restrictive cardiomyopathy (0.4), and infective endocarditis (0.1) were the main disease etiologies. Mortality rate per 100-person years of follow-up varied from 13.8 (95% CI: 6.2-30.7) in peri-partum cardiomyopathy to 92.9 (46.5-185.9) in infective endocarditis. Compared to ischemic heart disease, the mortality was two to five times higher in rheumatic heart disease (HR = 2.0; 95% CI: 1.6-2.4), congenital heart disease (2.9; 1.9-4.2), and infective endocarditis (4.8; 2.4-9.8). The wide variations in mortality rate in HF patients may bring possible clinical applicability of risk stratification., Competing Interests: Competing interests: P.J. is supported by a Wellcome Trust/DBT India Alliance Clinical and Public Health Senior Fellowship (IA/CPHS/20/1/505229). P.J. received research funding from the National Health and Medical Research Council—Australia (1160283 and 1169766), the Medical Research Council—UK (MR/T037822/1), the National Institute for Health and Care Research (NIHR 204871 and 201815), and the Indian Council of Medical Research., (© 2024. The Author(s).)

Heart failure (HF) is a condition with growing morbidity and mortality. Dyslipidemia in HF is not concentrated around hypercholesterolemia as in coronary artery disease. As a corollary, the robust benefits seen with statins across the spectrum of CAD have not been replicated in HF. Multiple potential pleiotropic effects of statins include anti-inflammatory, antioxidant, endothelial stabilization, antiapoptotic, anti-thrombotic, and modulation of the autonomic system apart from lipid lowering. These benevolent actions need to be counterbalanced with the potential derangement of ubiquinone, selenoprotein and endotoxin pathways. While small randomized and non-randomized studies demonstrated a multitude of benefits in clinical and surrogate endpoints, two large RCTs failed to demonstrate unequivocal benefits. However, multiple large meta-analyses do demonstrate definite improvement in clinical endpoints including death and heart failure hospitalization. The clinical likelihood of benefit was higher in younger patients with less advanced HF and use of lipophilic statins.

Aims: Limited data on the uptake of guideline-directed medical therapies (GDMTs) and the mortality of acute decompensated HF (ADHF) patients are available from India. The National Heart Failure Registry (NHFR) aimed to assess clinical presentation, practice patterns, and the mortality of ADHF patients in India., Methods and Results: The NHFR is a facility-based, multi-centre clinical registry of consecutive ADHF patients with prospective follow-up. Fifty three tertiary care hospitals in 21 states in India participated in the NHFR. All consecutive ADHF patients who satisfied the European Society of Cardiology criteria were enrolled in the registry. All-cause mortality at 90 days was the main outcome measure. In total, 10 851 consecutive patients were recruited (mean age: 59.9 years, 31% women). Ischaemic heart disease was the predominant aetiology for HF (72%), followed by dilated cardiomyopathy (18%). Isolated right HF was noted in 62 (0.6%) participants. In eligible HF patients, 47.5% received GDMT. The 90 day mortality was 14.2% (14.9% and 13.9% in women and men, respectively) with a re-admission rate of 8.4%. An inverse relationship between educational class based on years of education and 90 day mortality (high mortality in the lowest educational class) was observed in the study population. Patients with HF with reduced ejection fraction and HF with mildly reduced ejection fraction who did not receive GDMT experienced higher mortality (log-rank P < 0.001) than those who received GDMT. Baseline educational class, body mass index, New York Heart Association functional class, ejection fraction, dependent oedema, serum creatinine, QRS > 120 ms, atrial fibrillation, mitral regurgitation, haemoglobin levels, serum sodium, and GDMT independently predicted 90 day mortality., Conclusion: One of seven ADHF patients in the NHFR died during the first 90 days of follow-up. One of two patients received GDMT. Adherence to GDMT improved survival in HF patients with reduced and mildly reduced ejection fractions. Our findings call for innovative quality improvement initiatives to improve the uptake of GDMT among HF patients in India., (© 2022 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)

Objective: Heart failure (HF) has emerged as a global public health problem that affects both low and high-income countries. The high HF burden and the need for resource-intensive treatments often lead to health system crisis in resource-poor settings. Data on prevailing practice patterns and long-term clinical outcomes of HF are scarce from the low and middle-income countries. Nationally representative HF data from India are not available., Methods: The National Heart Failure Registry (NHFR) is a multicentric, hospital-based registry of HF patients from 53 centers across India. Consecutive patients admitted with the diagnosis of acute decompensated HF satisfying the European Society of Cardiology (ESC) 2016 criteria will be enrolled into the registry from January 2019 to December 2019. Each participating center is expected to contribute 200 patients into the registry (i.e., more than 10,000 HF patients from India). We are collecting demographics, clinical, laboratory, imaging, and other diagnostic data at baseline from all registered patients in the registry by using a structured document. Additionally, we are collecting the details of treatment practices and the usage of guideline-directed therapy from all participants. We intend to obtain the in-hospital, 3-months, 6-months and one-year outcome data on mortality, cause of death, and repeated hospitalization events., Conclusions: In summary, NFHR will be the first nationally representative HF registry aimed at providing crucial information on prevailing etiology, distribution and current practices in the management of HF., Competing Interests: Conflicts of interest The authors have none to declare. Panniyammakal Jeemon was supported by the Wellcome Trust/DBT India Alliance Fellowship [grant number IA/CPHI/14/1/501497]. ICMR – Indian Council for Medical Research is funding the study., (Copyright © 2020 Cardiological Society of India. Published by Elsevier B.V. All rights reserved.)

Heart failure is a common clinical syndrome and a global health priority. The burden of heart failure is increasing at an alarming rate worldwide as well as in India. Heart failure not only increases the risk of mortality, morbidity and worsens the patient's quality of life, but also puts a huge burden on the overall healthcare system. The management of heart failure has evolved over the years with the advent of new drugs and devices. This document has been developed with an objective to provide standard management guidance and simple heart failure algorithms to aid Indian clinicians in their daily practice. It would also inform the clinicians on the latest evidence in heart failure and provide guidance to recognize and diagnose chronic heart failure early and optimize management., (Copyright © 2017. Published by Elsevier B.V.)

Introduction: Although diuretics are mainly used for the treatment of acute decompensated heart failure (ADHF), inadequate responses and complications have led to the use of extracorporeal ultrafiltration (UF) as an alternative strategy for reducing volume overloads in patients with ADHF., Objective: The aim of our study is to perform meta-analysis of the results obtained from studies on extracorporeal venous ultrafiltration and compare them with those of standard diuretic treatment for overload volume reduction in acute decompensated heart failure., Methods: MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials databases were systematically searched using a pre‑specified criterion. Pooled estimates of outcomes after 48 h (weight change, serum creatinine level, and all-cause mortality) were computed using random effect models. Pooled weighted mean differences were calculated for weight loss and change in creatinine level, whereas a pooled risk ratio was used for the analysis of binary all-cause mortality outcome., Results: A total of nine studies, involving 613 patients, met the eligibility criteria. The mean weight loss in patients who underwent UF therapy was 1.78 kg [95% Confidence Interval (CI): -2.65 to -0.91 kg; p < 0.001) more than those who received standard diuretic therapy. The post-intervention creatinine level, however, was not significantly different (mean change = -0.25 mg/dL; 95% CI: -0.56 to 0.06 mg/dL; p = 0.112). The risk of all-cause mortality persisted in patients treated with UF compared with patients treated with standard diuretics (Pooled RR = 1.00; 95% CI: 0.64-1.56; p = 0.993)., Conclusion: Compared with standard diuretic therapy, UF treatment for overload volume reduction in individuals suffering from ADHF, resulted in significant reduction of body weight within 48 h. However, no significant decrease of serum creatinine level or reduction of all-cause mortality was observed.

Idiopathic aneurysmal dilatations of the right atrium are rare anomalies. We report one such case of a young man presenting with fatigue, abdominal distension, pedal oedema, unremarkable cardiac examination except for raised jugular venous pressure, an electrocardiogram showing normal sinus rhythm with right bundle-branch block, and an radiograph of the chest showing cardiomegaly. The echocardiographic examination revealed a giant right atrium with low pressure tricuspid regurgitation. The computed tomography confirmed the findings of two-dimensional echocardiography. He was put on medical treatment and remained symptomatically controlled on follow-up., (Copyright © 2012 Cardiological Society of India. Published by Elsevier B.V. All rights reserved.)

It is now well known that congestive heart failure (CHF) is invariably associated with cardiac hypertrophy, and changes in the shape and size of cardiomyocytes (cardiac remodeling) are considered to explain cardiac dysfunction in CHF. However, the mechanisms responsible for the transition of cardiac hypertrophy to heart failure are poorly understood. Several lines of evidence both from various experimental models of CHF and from patients with different types of CHF have indicated that the functions of different subcellular organelles such as extracellular matrix, sarcolemma, sarcoplasmic reticulum, myofibrils, mitochondria, and nucleus are defective. Subcellular abnormalities for protein contents, gene expression, and enzyme activities in the failing heart become evident as a consequence of prolonged hormonal imbalance, metabolic derangements, and cation maldistribution. In particular, the occurrence of oxidative stress, development of intracellular Ca2+ overload, activation of proteases and phospholipases, and alterations in cardiac gene expression result in changes in the biochemical composition, molecular structure, and function of different subcellular organelles (subcellular remodeling). Not only does subcellular remodeling appear to be intimately involved in the transition of cardiac hypertrophy to heart failure, the mismatching of the function of different subcellular organelles leads to the development of cardiac dysfunction. Although blockade of the renin-angiotensin system, sympathetic nervous system, and various other hormonal actions have been reported to produce beneficial effects on cardiac remodeling and heart dysfunction in CHF, the actions of various cardiac drugs on subcellular remodeling have not been examined extensively. Some recent studies have indicated that both the angiotensin-converting enzyme inhibitors and angiotensin receptor antagonists attenuate changes in sarcolemma, sarcoplasmic reticulum, and myofibril enzyme activities, protein contents, and gene expression, and partly improve cardiac function in the failing hearts. It is suggested that subcellular remodeling is an excellent target for the development of improved drug therapy for CHF. Furthermore, extensive studies should investigate the effects of different agents individually or in combination on reverse subcellular remodeling, cardiac remodeling, and cardiac dysfunction in various experimental models of CHF.

Earlier studies have revealed an improvement of cardiac function in animals with congestive heart failure (CHF) due to myocardial infarction (MI) by treatment with angiotensin converting enzyme (ACE) inhibitors. Since heart failure is also associated with attenuated responses to catecholamines, we examined the effects of imidapril, an ACE inhibitor, on the beta-adrenoceptor (beta-AR) signal transduction in the failing heart. Heart failure in rats was induced by occluding the coronary artery, and 3 weeks later the animals were treated with g/(kg x day) (orally) imidapril for 4 weeks. The animals were assessed for their left ventricular function and inotropic responses to isoproterenol. Cardiomyocytes and crude membranes were isolated from the non-ischemic viable left ventricle and examined for the intracellular concentration of Ca2+ [Ca2+]i and beta-ARs as well as adenylyl cyclase (AC) activity, respectively. Animals with heart failure exhibited depressions in ventricular function and positive inotropic response to isoproterenol as well as isoproterenol-induced increase in [Ca2+]i in cardiomyocytes; these changes were attenuated by imidapril treatment. Both beta1-AR receptor density and isoproterenol-stimulated AC activity were decreased in the failing heart and these alterations were prevented by imidapril treatment. Alterations in cardiac function, positive inotropic effect of isoproterenol, beta1-AR density and isoproterenol-stimulated AC activity in the failing heart were also attenuated by treatment with another ACE inhibitor, enalapril and an angiotensin II receptor antagonist, losartan. The results indicate that imidapril not only attenuates cardiac dysfunction but also prevents changes in beta-AR signal transduction in CHF due to MI. These beneficial effects are similar to those of enalapril or losartan and thus appear to be due to blockade of the renin-angiotensin system.

Objectives: Earlier studies have revealed beneficial effects of metabolic therapy in animals with congestive heart failure (CHF) due to myocardial infarction. Because heart failure is also associated with attenuated response to catecholamines, we examined the effects of propionyl L-carnitine (PLC) (a carnitine derivative) therapy on the beta-adrenoceptor (beta-AR) signal transduction in the failing heart., Methods: Heart failure in rats was induced by occluding the coronary artery and 3 weeks later the animals were treated with or without 100 mg/kg (intraperitoneally, daily) PLC for 5 weeks. The animals were assessed for their left ventricular function and inotropic responses to isoproterenol. Crude membranes were isolated from the remote, nonischemic (viable) left ventricle and examined for changes in beta-AR and adenylyl cyclase (AC) activity., Results: Animals with heart failure exhibited depressions in ventricular function, positive inotropic response to isoproterenol, beta-AR receptor density and basal AC activity; these changes were also attenuated by PLC treatment. The stimulation of AC activities with isoproterenol, 5'-guanyl imidodiphosphate, forskolin and sodium fluoride was decreased in the failing hearts and these changes were also prevented by PLC treatment., Conclusion: The results indicate that metabolic therapy with PLC not only attenuates the defects in heart function but also prevents changes in the beta-AR signal transduction in CHF due to myocardial infarction., (Copyright 2004 Lippincott Williams & Wilkins)

Cardiac dysfunction in animals with congestive heart failure due to myocardial infarction (MI) is known to be associated with a wide variety of defects in receptor and post-receptor mechanisms. Since the heart function have been shown to be improved by treatment with different angiotensin converting enzyme (ACE) inhibitors, we examined the effects of imidapril, an ACE inhibitor, on changes in post-receptor mechanisms involving adenylyl cyclase (AC) and G proteins in the failing heart. Heart failure in rats was induced by occluding the coronary artery and 3 weeks later the animals were treated daily with 1 mg/kg (orally) imidapril for 5 weeks. The animals were assessed for their left ventricular function and crude membranes were isolated from the viable left ventricle and examined for AC activities as well as G-protein activities and expression. Animals with heart failure exhibited depressions in ventricular function and AC activities in the absence or presence of forskolin, NaF and Gpp(NH)p. The AC activity in the presence of pertussis toxin was increased whereas that in the presence of cholera toxin was decreased in the failing heart. Protein contents and mRNA levels for G(i)-proteins were increased whereas those for G(s)-proteins were unaltered in the infarcted heart. All these changes due to MI were prevented by imidapril treatment. The results indicate that the depressed cardiac function in the failing heart may partly be due to the direct effects of changes in AC and G(i) proteins.

Objective: Earlier studies have revealed sarcolemmal (SL) defects in congestive heart failure due to myocardial infarction; however, the mechanisms of SL changes in the failing heart are poorly understood. Since congestive heart failure is associated with various metabolic abnormalities including a deficiency of carnitine, we examined the effects of propionyl L-carnitine, a carnitine derivative, in animals with congestive heart failure., Methods: For this purpose, heart failure in rats was induced by occluding the coronary artery and 3 weeks later the animals were treated with 100 mg/kg (i.p. daily) propionyl L-carnitine for 4 weeks. The sham control group received saline injections. The animals were assessed for their left ventricular function. SL membranes were examined for Na(+)-K+ ATPase, Na(+)-Ca2+ exchange and adenylate cyclase activities., Results: A marked improvement in the attenuated left ventricular function of the experimental animals was seen upon treatment with propionyl L-carnitine. The SL adenylyl cyclase activities in control, untreated failing hearts and treated failing hearts were 590 +/- 36, 190 +/- 22 and 320 +/- 21 pmol cAMP/mg/10 min, whereas the SL Na(+)-K+ ATPase activities were 35.7 +/- 2.8, 22.5 +/- 2.4 and 30.1 +/- 2.8 mumol Pi/mg/h, respectively. Furthermore, the SL Na(+)-dependent Ca(2+)-uptake activity, which decreased in the failing hearts (4.6 +/- 0.4 vs. 9.3 +/- 0.7 nmol Ca2+/mg/2 s for control), was improved (6.8 +/- 0.5 nmol Ca2+/mg/2 s) significantly following treatment with propionyl L-carnitine., Conclusion: These results indicate that metabolic therapy with propionyl L-carnitine may attenuate defects in the SL membrane and thus may improve heart function in congestive heart failure due to myocardial infarction.

In order to examine the status of G-proteins in congestive heart failure due to myocardial infarction, the left coronary artery in rats was ligated and animals assessed after 4, 8 and 16 weeks. Sham-operated control and experimental animals were used for the preparation of membranes from the viable (uninfarcted) left and right ventricles. Adenylyl cyclase activities in the presence of pertussis toxin and cholera toxin were increased and decreased in left ventricles from all groups, respectively. On the other hand, adenylyl cyclase activities in 8 and 16-week experimental right ventricles were unaltered in the presence of pertussis toxin and increased in the presence of cholera toxin. Depression of adenylyl cyclase activities in left ventricles from all groups as well as in the right ventricle at 4 weeks were not evident when enzyme activity was determined in the pertussis toxin-treated membranes in the absence or presence of Gpp(NH)p. Cholera toxin-catalyzed ADP ribosylation was decreased in left ventricles from all infarcted groups and increased in the right ventricles at 8 and 16 weeks whereas the pertussis toxin-catalyzed ADP ribosylation was increased in all experimental tissues except in the right ventricles at 8 and 16 weeks. G(s alpha)-protein content was decreased in the left ventricle at 16 weeks and increased in the right ventricles at 8 and 16 weeks of myocardial infarction. On the other hand, G(i alpha)-protein content was increased in left ventricles from all infarcted groups and the 4-week right ventricle but was unaltered in 8 and 16-week right ventricles. An increase in mRNA abundance for G(i alpha)-protein was seen in both left and right ventricles following myocardial infarction. A significant increase in mRNA level for G(s alpha)-protein was observed in all left ventricles and 8-week right ventricle following the coronary occlusion. These results suggest that changes in Gs- and Gi-proteins in the failing heart due to myocardial infarction are chamber-specific and are dependent upon the stage of congestive heart failure.

The status of beta-adrenergic receptors and adenylyl cyclase in crude membranes from both left and right ventricles was examined when the left coronary artery in rats was occluded for 4, 8, and 16 wk. The adenylyl cyclase activity in the presence of isoproterenol was decreased in the uninfarcted (viable) left ventricle and increased in the right ventricle subsequent to myocardial infarction. The density of beta1-adrenergic receptors, unlike beta2-receptors, was reduced in the left ventricle, whereas no change in the characteristics of beta1- and beta2-adrenergic receptors was seen in the right ventricle. The catalytic activity of adenylyl cyclase was depressed in the viable left ventricle but was unchanged in the right ventricle. In comparison to sham controls, the basal, as well as NaF-, forskolin-, and 5'-guanylyl imidodiphosphate [Gpp(NH)p]-stimulated adenylyl cyclase activities were decreased in the left ventricle and increased in the right ventricle of the experimental animals. Opposite alterations in the adenylyl cyclase activities in left and right ventricles from infarcted animals were also seen when two types of purified sarcolemmal preparations were employed. These changes in adenylyl cyclase activities in the left and right ventricles were dependent on the degree of heart failure. Furthermore, adenosine 3',5'-cyclic monophosphate contents were higher in the right ventricle and lower in the left ventricle from infarcted animals injected with saline, isoproterenol, or forskolin in comparison to the controls. The results suggest differential changes in the viable left and right ventricles with respect to adenylyl cyclase activities during the development of congestive heart failure due to myocardial infarction.

In view of the lack of information regarding the status of beta-adrenoceptor mediated signal transduction mechanisms at severe stages of congestive heart failure, the status of beta-adrenoceptors, G-proteins and adenylyl cyclase activities was examined in 220-275 day old cardiomyopathic hamster hearts. Although no changes in the Kd values for beta 1- and beta 2-adrenoceptors were seen, the number of beta 1-adrenoceptors, unlike that of beta 2-adrenoceptors, was markedly decreased in cardiac membranes from failing hearts. The activation of adenylyl cyclase in the failing hearts by different concentrations of isoproterenol was also attenuated in comparison to the control preparations. The basal adenylyl cyclase activity in cardiac membranes from the failing hearts was not altered; however, the stimulated enzyme activities, when measured in the presence of forskolin, NaF or Gpp(NH)p were depressed significantly. The functional activity of Gs-proteins (measured by cholera toxin stimulation of adenylyl cyclase) was depressed whereas that of Gi-proteins (measured by pertussis toxin stimulation of adenylyl cyclase) was increased in the failing hearts. Not only were the Gs- and Gi-protein contents (measured by immunoblotting) increased, the bioactivities of these proteins as determined by ADP-ribosylations in the presence of cholera toxin and pertussis toxin, respectively, were also higher in failing hearts in comparison to the control values. Northern blot analysis revealed that the signals for Gs- and Gi-protein mRNAs were augmented at this stage of heart failure. These results indicate that the loss of adrenergic support at severe stages of congestive heart failure in cardiomyopathic hamsters may involve a reduction in the number of beta 1-adrenoceptors, and an increase in Gi-protein contents as well as bioactivities in addition to an uncoupling of Gs-proteins from the catalytic site of adenylyl cyclase in cardiac membrane.

It is well known that the positive inotropic effect of catecholamines is mediated through the activation of adrenergic receptors and the formation of cyclic adenosine monophosphate (AMP) in the cardiac cell. Although attenuated responses of failing hearts to catecholamines are commonly seen in patients and experimental animals with coronary artery disease, their mechanisms are poorly understood. To examine the status of beta-adrenergic receptors and postadrenergic receptor mechanisms in congestive heart failure due to myocardial infarction, the left coronary artery in rats was ligated for 4 and 8 weeks before studying the hemodynamic and biochemical changes due to isoproterenol, a beta-adrenoceptor agonist, or forskolin, a postreceptor agonist. Isolated perfused rat heart preparations were also used for studying changes in contractile function and cyclic AMP content. The hemodynamic actions and changes in the left ventricular cyclic AMP content in the experimental animals were depressed, not only in response to isoproterenol but also to forskolin. The density of beta-adrenoceptors was also decreased in the failing myocardium. In isolated perfused hearts from the 8-week experimental animals, isoproterenol-induced as well as forskolin-induced increases in both contractile force and cyclic AMP content in the left ventricle were depressed. These data suggest that defects in both beta-adrenergic receptor and postreceptor sites may be involved in attenuating the response of infarcted hearts to catecholamines.

In order to explain the attenuated sympathetic support during the development of heart failure, the status of beta-adrenergic mechanisms in the failing myocardium was assessed by employing cardiomyopathic hamsters (155-170 days old) at moderate degree of congestive heart failure. The norepinephrine turnover rate was increased but the norepinephrine content was decreased in cardiomyopathic hearts. The number and the affinity of beta receptors in the sarcolemmal preparations were not changed in these hearts at moderate stage of congestive heart failure. While the basal adenylyl cyclase activity was not altered in sarcolemma, the stimulation of enzyme activity by NaF, forskolin, Gpp(NH)p or epinephrine was depressed in hearts from these cardiomyopathic hamsters. Since G-proteins are involved in modifying the adenylyl cyclase activity, the functional and bioactivities as well as contents of both Gs and Gi proteins were determined in the cardiomyopathic heart sarcolemma. The functional stimulation of adenylyl cyclase by cholera toxin, which activates Gs proteins, was markedly depressed whereas that by Pertussis toxin, which inhibits Gi proteins, was markedly augmented in cardiomyopathic hearts. The cholera toxin and pertussis toxin catalyzed ADP-ribosylation was increased by 37 and 126%, respectively; this indicated increased bioactivities of both Gs and Gi proteins in experimental preparations. The immunoblot analysis suggested 74 and 124% increase in Gs and Gi contents in failing hearts, respectively. These results suggest that depressed adenylyl cyclase activation in cardiomyopathic hamsters may not only be due to increased content and bioactivity of Gi proteins but the functional uncoupling of Gs proteins from the adenylyl cyclase enzyme may also be involved at this stage of heart failure.

The rat model of myocardial infarction is characterized by progressive cardiac hypertrophy and failure. Rats with infarcts greater than 30% of the left ventricle exhibited early and moderate stages of heart failure 4 and 8 weeks after the occlusion of the left coronary artery, respectively. As heart failure is usually associated with remodeling of the extracellular matrix, a histological and biochemical study of cardiac collagenous proteins was carried out using failing hearts. Total collagen content in the right ventricle increased at 2, 4, and 8 weeks following occlusion of the left coronary artery whereas such a change in viable left ventricle was seen after 4 and 8 weeks. Total cardiac hydroxyproline concentration was increased in both right and left ventricular samples from the infarcted animals when compared to those of control; this increase was due to elevation of pepsin-insoluble collagen fraction. The myocardial noncollagenous/collagenous protein ratio was decreased in experimental right and left ventricular samples when compared to control samples. These findings suggest that an increase in cross-linking of cardiac collagen as well as disparate synthesis of collagenous and noncollagenous proteins occurs in this model of congestive heart failure.