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1.
The reverse metabolic syndrome in the elderly: Is it a "catabolic" syndrome?
Curcio, F, Sasso, G, Liguori, I, Ferro, G, Russo, G, Cellurale, M, Della-Morte, D, Gargiulo, G, Testa, G, Cacciatore, F, et al
Aging clinical and experimental research. 2018;(6):547-554
Abstract
Traditional risk factors of cardiovascular death in the general population, including body mass index (BMI), serum cholesterol, and blood pressure are also found to relate to outcomes in the geriatric population, but in a differing direction. A higher body mass index, hypercholesterolemia and hypertension are not harmful but even permit better survival at advancing age. This phenomenon is called "reverse epidemiology" or "risk factor paradox" and is also detected in a variety of chronic disease states such as chronic heart failure. Accordingly, a low BMI, blood pressure and cholesterol values are associated with a worse prognosis. Several possible causes are hypothesized to explain this elderly paradox, but this phenomenon remains controversial and its underlying reasons are poorly understood. The aim of this review is to recognize the factors behind this intriguing phenomenon and analyse the consequences that it can bring in the management of the cardiovascular therapy in elderly patient. Finally, a new phenotype identified as "catabolic syndrome" has been postulated.
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2.
[Vitamin D deficiency, left ventricular dysfunction and heart failure].
Cioffi, G, Gatti, D, Adami, S
Giornale italiano di cardiologia (2006). 2010;(9):645-53
Abstract
Epidemiologic data indicate that about one million people worldwide suffer from and should be treated for vitamin D deficiency. The clinical impact of vitamin D deficiency is very high if we consider the pivotal role that this condition plays in determining osteoporosis, fractures, cancers, diabetes, vascular inflammation, which can severely reduce functional capacity, quality of life and may often lead to disability. Vitamin D deficiency is a widely underdiagnosed pathological condition. Although many cardiovascular diseases such as arterial hypertension, myocardial ischemia, diabetic cardiomyopathy and heart failure, may arise from a low vitamin D status, cardiologists do not routinely search for this disease in clinical practice. Vitamin D, indeed, stimulates the synthesis of various contractile proteins and activates crucial intracellular mechanisms that manage calcium metabolism and energy production. These functions can be altered once vitamin D deficiency develops. This review focuses on the relationship between vitamin D deficiency, asymptomatic changes in left ventricular geometry and function, and heart failure syndrome through a recall of the myocardial metabolic processes regulated by vitamin D. The analysis of the available data from the literature leads to raise some questions that, at present, have no answer. Future prospective studies are needed to assess the effect of treatment of vitamin D deficiency on cardiac function.
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3.
Comparison of 80 versus 10 mg of atorvastatin on occurrence of cardiovascular events after the first event (from the Treating to New Targets [TNT] trial).
LaRosa, JC, Deedwania, PC, Shepherd, J, Wenger, NK, Greten, H, DeMicco, DA, Breazna, A, ,
The American journal of cardiology. 2010;(3):283-7
Abstract
Analyses of randomized clinical trials are usually restricted to examination of time to first event. However, because many patients have multiple events, this approach precludes much potentially useful clinical and economic data. To assess the effect on overall disease burden in the Treating to New Targets (TNT) study, we evaluated the effect of treatment with atorvastatin 80 versus 10 mg in the period after the occurrence of a first cardiovascular event. In TNT, 10,001 patients with stable coronary heart disease received double-blind therapy with atorvastatin 80 or 10 mg and were followed for 4.9 years. Post hoc time-to-event analysis was used to estimate separate hazard ratios for time to any first, second, third, fourth, and fifth recurrent cardiovascular events. During TNT, 3,082 patients had a first recurrent cardiovascular event, with 1,516, 698, 345, and 197 developing second, third, fourth, and fifth recurrent events, respectively. In patients receiving atorvastatin 80 mg, the relative risk of a first recurrent event was significantly decreased compared to those receiving atorvastatin 10 mg. Significant benefit with the 80-mg dose was also observed for second, third, fourth, and fifth recurrent events. Similar findings were recorded in 5,854 patients with type 2 diabetes mellitus and/or metabolic syndrome and in 3,809 patients > or = 65 years of age compared to younger patients. In conclusion, treatment with atorvastatin 80 mg continued to significantly decrease the risk of any cardiovascular event over time compared to atorvastatin 10 mg in patients who had survived previous events. In TNT, analyses limited to the primary end point significantly underestimated the decrease in total cardiovascular disease burden achieved by intensive low-density lipoprotein cholesterol lowering.
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4.
ALLHAT findings revisited in the context of subsequent analyses, other trials, and meta-analyses.
Wright, JT, Probstfield, JL, Cushman, WC, Pressel, SL, Cutler, JA, Davis, BR, Einhorn, PT, Rahman, M, Whelton, PK, Ford, CE, et al
Archives of internal medicine. 2009;(9):832-42
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Abstract
The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) is reevaluated considering information from new clinical trials, meta-analyses, and recent subgroup and explanatory analyses from ALLHAT, especially those regarding heart failure (HF) and the association of drug treatment with new-onset diabetes mellitus (DM) and its cardiovascular disease (CVD) consequences. Chlorthalidone was superior to (1) doxazosin mesylate in preventing combined CVD (CCVD) (risk ratio [RR], 1.20; 95% confidence interval [CI], 1.13-1.27), especially HF (RR, 1.80; 95% CI, 1.40-2.22) and stroke (RR, 1.26; 95% CI, 1.10-1.46); (2) lisinopril in preventing CCVD (RR, 1.10; 95% CI, 1.05-1.16), including stroke (in black persons only) and HF (RR, 1.20; 95% CI, 1.09-1.34); and (3) amlodipine besylate in preventing HF, overall (by 28%) and in hospitalized or fatal cases (by 26%). Central independent blinded reassessment of HF hospitalizations confirmed each comparison. Results were consistent by age, sex, race (except for stroke and CCVD), DM status, metabolic syndrome status, and renal function level. Neither amlodipine nor lisinopril was superior to chlorthalidone in preventing end-stage renal disease overall, by DM status, or by renal function level. In the chlorthalidone arm, new-onset DM was not significantly associated with CCVD (RR, 0.96; 95% CI, 0.88-2.42). Evidence from subsequent analyses of ALLHAT and other clinical outcome trials confirm that neither alpha-blockers, angiotensin-converting enzyme inhibitors, nor calcium channel blockers surpass thiazide-type diuretics (at appropriate dosage) as initial therapy for reduction of cardiovascular or renal risk. Thiazides are superior in preventing HF, and new-onset DM associated with thiazides does not increase CVD outcomes.
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5.
The pathophysiology of cardiac cachexia.
Freeman, LM
Current opinion in supportive and palliative care. 2009;(4):276-81
Abstract
PURPOSE OF REVIEW Cardiac cachexia, the loss of lean body mass that affects a large proportion of patients with chronic heart failure, is associated with increased morbidity and mortality. The pathophysiology of cardiac cachexia is complex and multifactorial, but recent studies are providing new information that is helping to clarify the pathophysiology and new targets for treatment. RECENT FINDINGS New attention is being paid to developing a definition as well as a clinically relevant way to diagnose this syndrome. The adverse clinical effects of cachexia are being emphasized by new research on the obesity paradox, suggesting that cardiac cachexia is such a detrimental process that obesity actually confers a survival benefit. This information is useful in developing practical approaches to managing body weight and lean tissue in chronic heart failure patients and may provide therapeutic targets. New mechanisms and pathways that mediate cardiac cachexia are being identified and appear to act by increasing energy requirements, reducing energy intake, impairing nutrient absorption, and causing metabolic alterations. SUMMARY Recent studies have helped to better delineate multifactorial mechanisms in the pathophysiology of cardiac cachexia that may lead to more effective treatments to address this common and important syndrome in patients with chronic heart failure.
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Impairment in walking capacity and myocardial function in the elderly: is there a role for nonpharmacologic therapy with nutritional amino acid supplements?
Scognamiglio, R, Testa, A, Aquilani, R, Dioguardi, FS, Pasini, E
The American journal of cardiology. 2008;(11A):78E-81E
Abstract
Elderly persons have reduced muscular mass, with consequent deterioration of their daily activities and reduced quality of life. This is more pronounced in elderly patients affected by chronic diseases such as chronic heart failure (CHF). It has been demonstrated that oral amino acid (AA) supplementation improves muscle protein metabolism. A recent study shows that use of oral supplements with a special mixture of AAs for 12 weeks increases (1) 6-minute walk distance (from 212.5 +/- 34 m to 268.8 +/- 34.9 m; p <0.001), (2) maximal isometric muscular strength (from 14.6 +/- 2.2 kg to 20.2 +/- 2 kg; p <0.001), and (3) peak exercise left ventricular ejection fraction (LVEF 0.55 + 0.4 vs 0.67 + 0.7) (0.558 vs 0.67 +/- 0.7; p <0.01). In a pilot observational study, we studied elderly patients with CHF who were clinically stable on standard therapy (age range, 68-76 years; New York Heart Association (NYHA) class II-III; LVEF <0.40; normal body mass index and arm muscle measurements; peak oxygen consumption <15 mL/kg per min). After basal assessment of (1) cardiac function (by 2-dimensional echocardiography), (2) 6-minute walk test, and (3) blood variables, an AA mixture (4 g x 2 die) was orally administered to the patients for 12 weeks in conjunction with standard therapies and a controlled diet. The AA supplements increased 6-minute walk distance significantly (201 +/- 12 m vs 226 +/- 9 m; p < 0.05). Interestingly, urea values were unchanged (31.3 +/- 10.5 mg/dL vs 32.4 +/- 8.1 mg/dL; p = NS). Our results suggest the potential role of a nonpharmacologic therapy with nutrients (ie, AAs) in an attempt to improve muscular metabolism and function in elderly subjects and in hypercatabolic syndromes such as CHF.
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7.
Emerging therapies for the management of decompensated heart failure: from bench to bedside.
deGoma, EM, Vagelos, RH, Fowler, MB, Ashley, EA
Journal of the American College of Cardiology. 2006;(12):2397-409
Abstract
While pharmaceutical innovation has been highly successful in reducing mortality in chronic heart failure, this has not been matched by similar success in decompensated heart failure syndromes. Despite outstanding issues over definitions and end points, we argue in this paper that an unprecedented wealth of pharmacologic innovation may soon transform the management of these challenging patients. Agents that target contractility, such as cardiac myosin activators and novel adenosine triphosphate-dependent transmembrane sodium-potassium pump inhibitors, provide inotropic support without arrhythmogenic increases in cytosolic calcium or side effects of more traditional agents. Adenosine receptor blockade may improve glomerular filtration and diuresis by exerting a direct beneficial effect on glomerular blood flow while vasopressin antagonists promote free water excretion without compromising renal function and may simultaneously inhibit myocardial remodeling. Urodilatin, the renally synthesized isoform of atrial natriuretic peptide, may improve pulmonary congestion via vasodilation and enhanced diuresis. Finally, metabolic modulators such as perhexiline may optimize myocardial energy utilization by shifting adenosine triphosphate production from free fatty acids to glucose, a unique and conceptually appealing approach to the management of heart failure. These advances allow optimism not only for the advancement of our understanding and management of decompensated heart failure syndromes but for the translational research effort in heart failure biology in general.
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8.
Prognosis and therapy approaches of cardiac cachexia.
Springer, J, Filippatos, G, Akashi, YJ, Anker, SD
Current opinion in cardiology. 2006;(3):229-33
Abstract
PURPOSE OF REVIEW This review focuses on the prognostic implications and therapeutic approaches in cardiac cachexia - a syndrome that has been recognized for a long time, although it has only received increased attention lately. RECENT FINDINGS Cardiac cachexia is a common and serious complication of chronic heart failure and associated with very poor prognosis, yet is often recognized by the clinicians only at late stage. Approximately 15% of heart failure patients will develop cardiac cachexia, defined by a 6% non-edematous, non-voluntary weight loss over a period of 6 months. Several studies have demonstrated that cardiac cachexia is a multi-factorial disease, which involves increased neurohormonal activity and immune abnormalities, resulting in hormonal and metabolic catabolic/anabolic imbalance of the body, leading to the loss of fat and lean mass and ultimately death. So far, there are no standardized therapies available for this disease. SUMMARY Cardiac cachexia in heart failure patients is under-recognized and there is currently no causal therapy available. Several interesting treatment options exist, however, which have emerged recently, including appetite stimulants, hormones and 'classical' drugs, such as beta-blockers and ACE inhibitors.