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Heart Failure

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Response to letter regarding article, "combined cardiac magnetic resonance imaging and C-reactive protein levels identify a cohort at low risk for defibrillator firings and death".
By: Wu KC, Gerstenblith G, Marine JE, Dalal D, Cheng A, Lima JA, Tomaselli GF, Weiss RG, Guallar E, Marbán E.

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Intracoronary cardiosphere-derived cells for heart regeneration after myocardial infarction (CADUCEUS): a prospective, randomized phase 1 trial.
By: Makkar RR, Smith RR, Cheng K, Malliaras K, Thomson LE, Berman D, Czer LS, Marbán L, Mendizabal A, Johnston PV, Russell SD, Schuleri KH, Lardo AC, Gerstenblith G, Marbán E.
Cardiosphere-derived cells (CDCs) reduce scarring after myocardial infarction, increase viable myocardium, and boost cardiac function in preclinical models. We show that intracoronary infusion of autologous CDCs in patients within six weeks of a MI is safe and decreased infarct size and increased viable myocardium. These findings are consistent with regeneration of myocardium and merit additional assessment in further clinical trials.
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Combined cardiac magnetic resonance imaging and C-reactive protein levels identify a cohort at low risk for defibrillator firings and death.
By: Wu KC, Gerstenblith G, Guallar E, Marine JE, Dalal D, Cheng A, Marbán E, Lima JA, Tomaselli GF, Weiss RG.
Annually, ~80,000 Americans receive guideline-based primary prevention implantable cardioverter-defibrillators (ICDs), but appropriate firing rates are low. In a cohort of primary prevention ICD candidates, combining a myocardial heterogeneity index with an inflammatory biomarker identified a subgroup with a very low risk for adverse cardiac events, including ventricular arrhythmias. This novel approach warrants further investigation to confirm its value as a clinical risk stratification tool.
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Allopurinol acutely increases adenosine triphosphate energy delivery in failing human hearts.
By: Hirsch GA, Bottomley PA, Gerstenblith G, Weiss RG.
Intravenous administration of the XO inhibitor allopurinol acutely improves the relative and absolute concentrations of myocardial high-energy phosphates and ATP flux through creatine kinase (CK) in the failing human heart, offering direct evidence that myofibrillar CK energy delivery can be pharmaceutically augmented in the failing human heart.
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Creatine kinase-mediated improvement of function in failing mouse hearts provides causal evidence the failing heart is energy starved.
By: Gupta A, Akki A, Wang Y, Leppo MK, Chacko VP, Foster DB, Caceres V, Shi S, Kirk JA, Su J, Lai S, Paolocci N, Steenbergen C, Gerstenblith G, Weiss RG.
It has long been hypothesized that reduced energy delivery contributes to the contractile dysfunction of heart failure (HF). These observations provide direct evidence that the failing heart is “energy starved” as it relates to cardiac CK. In addition, these data identify CK as a promising therapeutic target for preventing and treating HF and possibly diseases involving energy-dependent dysfunction in other organs with temporally varying energy demands.
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Use of the Frank-Starling mechanism during exercise is linked to exercise-induced changes in arterial load.
By: Chantler PD, Melenovsky V, Schulman SP, Gerstenblith G, Becker LC, Ferrucci L, Fleg JL, Lakatta EG, Najjar SS.
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Polymorphisms of the beta adrenergic receptor predict left ventricular remodeling following acute myocardial infarction.
By: McLean RC, Hirsch GA, Becker LC, Kasch-Semenza L, Gerstenblith G, Schulman SP.
Prior studies demonstrate an association between specific beta-adrenergic receptor (?-AR) polymorphisms and clinical outcomes in patients with chronic heart failure and following acute coronary syndromes. The underlying mechanism may be due to differences in left ventricular remodeling. This study was undertaken to explore the relationship between LV remodeling after myocardial infarction and polymorphisms in the cardiac ?1-AR and ?2-AR genes. We found that polymorphisms of the ?1-AR and ?2-AR genes are associated with differential LV remodeling in patients treated with a ?1 receptor antagonist following ST-segment elevation myocardial infarction.
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Abnormalities in arterial-ventricular coupling in older healthy persons are attenuated by sodium nitroprusside.
By: Chantler PD, Nussbacher A, Gerstenblith G, Schulman SP, Becker LC, Ferrucci L, Fleg JL, Lakatta EG, Najjar SS.
The coupling between arterial elastance (E(A); net afterload) and left ventricular elastance (E(LV); pump performance), known as E(A)/E(LV), is a key determinant of cardiovascular performance and shifts during exercise due to a greater increase in E(LV) versus E(A). This normal exercise-induced reduction in E(A)/E(LV) decreases with advancing age. In conclusion, some age-associated deficiencies in E(A)/E(LV), E(A), and E(LV), in older subjects can be acutely abolished by single-nucleotide polymorphisms (SNPs) infusion. This is relevant to common conditions in older subjects associated with a significant impairment of exercise performance such as frailty or heart failure with preserved ejection fraction.
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Cardiovascular imaging for assessing cardiovascular risk in asymptomatic men versus women: the multi-ethnic study of atherosclerosis (MESA).
By: Jain A, McClelland RL, Polak JF, Shea S, Burke GL, Bild DE, Watson KE, Budoff MJ, Liu K, Post WS, Folsom AR, Lima JA, Bluemke DA.
CAC, carotid IMT, and LV mass and geometry offer the potential to characterize incident CVD risk in clinically asymptomatic individuals. The objective of the study was to compare these cardiovascular imaging measures for their overall and sex-specific ability to predict CVD. The study sample consisted of 4,965 MESA participants (48% men; mean age, 62±10 years). There was no evidence that imaging measures differed in association with incident CVD by sex. CAC was most strongly associated with CHD and CVD; LV mass and LV concentric remodeling best predicted stroke; and LV mass best predicted HF.
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Long-term effects of stem cell transplantation in the postinfarct heart: benefits and mechanisms.
By: Gerstenblith G, Weiss RG.

Long-term effects of stem cell transplantation in the postinfarct heart: benefits and mechanisms.

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