[Cardiac contractility modulation in heart failure with reduced ejection fraction treatment].

Heart failure with reduced left ventricular ejection fraction (LV EF) (HFrEF) is a significant issue of health care due to increasing indexes of morbidity and mortality. The emergence of a number of drugs and implantable devices for the treatment of HFrEF has allowed improvement of patients' well-being and prognosis. However, high mortality and recurrent decompensated heart failure remain a substantial issue and stimulate the search for new methods of CHF treatment. Cardiac contractility modulation (CCM) is a method of managing patients with HFrEF. Available data from randomized clinical trials (RCT) indicate the efficacy of CCM in improvement of patients' well-being and quality of life. The question remains open: what effect does CCM have on LV reverse remodeling? Experimental data and results of observational studies suggest a possibility of reverse remodeling by CCM; however, this has not been confirmed in RCT. Also, it remains unclear how CCM influences the frequency of hospitalizations for decompensated heart failure and the death rate of patients with HFrEF. Results of both RCTs and observational studies have shown a moderate improvement of quality of life associated with CCM. Furthermore, RCTs have not found any increase in LV EF due to the therapy, nor has a meta-analysis of RCTs revealed any improvement of the prognosis associated with CCM.  Further RCTs are needed to evaluate the effect of CCM on reverse remodeling, survival rate, and to determine the place of CCM in the treatment of patients with CHF.

Eligibility for sacubitril/valsartan in heart failure across the ejection fraction spectrum: real-world data from the Swedish Heart Failure Registry.

BACKGROUND: Randomized controlled trials (RCT) generalizability may be limited due to strict patient selection. OBJECTIVE: In a real-world heart failure (HF) population, we assessed eligibility for sacubitril/valsartan based on PARADIGM-HF (sacubitril/valsartan effective)/PARAGON-HF [sacubitril/valsartan effective in mildly reduced ejection fraction (EF)]. METHODS: Outpatients from the Swedish HF Registry (SwedeHF) were analysed. In SwedeHF, EF is recorded as <30, 30-39, 40-49 and ≥50%. In PARAGON-HF, sacubitril/valsartan was effective with EF ≤ 57% (i.e. median). We defined reduced EF/PARADIGM-HF as EF < 40%, mildly reduced EF/PARAGON-HF ≤ median as EF 40-49%, and normal EF/PARAGON-HF > median as EF ≥ 50%. We assessed 2 scenarios: (i) criteria likely to influence treatment decisions (pragmatic scenario); (ii) all criteria (literal scenario). RESULTS: Of 37 790 outpatients, 57% had EF < 40%, 24% EF 40-49% and 19% EF ≥ 50%. In the pragmatic scenario, 63% were eligible in EF < 50% (67% for EF < 40% and 52% for 40-49%) and 52% in EF ≥ 40% (52% for EF ≥ 50%). For the literal scenario, 32% were eligible in EF < 50% (38% of EF < 40%, 20% of EF 40-49%) and 22% in EF ≥ 40% (25% for EF ≥ 50%). Eligible vs. noneligible patients had more severe HF, more comorbidities and overall worse outcomes. CONCLUSION: In a real-world HF outpatient cohort, 81% of patients had EF < 50%, with 63% eligible for sacubitril/valsartan based on pragmatic criteria and 32% eligible based on literal trial criteria. Similar eligibility was observed for EF 40-49% and ≥50%, suggesting that our estimates for EF < 50% may be reproduced whether or not a higher cut-off for EF is considered.

[Prognostic value of liver stiffness in decompensated heart failure: results of prospective observational transient elastography-based study].

OBJECTIVE: There is growing evidence that liver stiffness (LS) in decompensated heart failure (DHF) is related to congestion, however data about its impact on outcomes are limited. The aim of the study was to evaluate associations and long-term prognostic significance of LS measured by transient elastography (TE) in DHF. METHODS: Single-center prospective observational study of 194 patients hospitalized with DHF, of whom 71 % were male, 68 ± 11 years (mean ± SD), had a left ventricular ejection fraction of 39±14%. LS by TE (FibroScan 502, Echosens, France) was measured on admission (n=176) and/or discharge (n=165). Outcomes of interest were all-cause death or heart transplantation, heart failure (HF) rehospitalisation, heart valve repair surgery. Outcome analysis was performed with Kaplan-Meier survival curves compared by log-rank test and with Cox proportional hazards regression. RESULTS: Median LS on admission and discharge were 11.1 (interquartile range 6.3;22.9) and 8.2 (5.8;14.0) kPa, respectively. Higher LS was associated with more clinical congestion on admission and discharge. Patients with LS on admission ≥11.1 kPa and at discharge ≥8.2 kPa were characterised by more pronounced clinical and echocardiographic signs of right-sided HF. Total of 5 (2.6%) patients died in hospital. Further, 31 (17.3%) deaths, 1 (0.6%) heart transplantation, 3 (1.7%) valve repair surgeries and 54 (30.2%) HF rehospitalizations occurred during follow-up (median 183 days). LS ≥ median was associated with higher probability of HF rehospitalizations and composite end point (all-cause death, heart transplantation, HF rehospitalisation and valve replacement therapy) both on admission (logrank p=0.004 and p=0.006) and at discharge (log-rank p=0.001 and p=0.004). Multivariable Cox regression analysis revealed that on a continuous scale LS increase per 1 kPa on admission was related to higher risk of HF hospitalization (hazard ratio [HR] 1.024, 95% confidential interval [CI] 1.002-1.046, p=0.03). LS at discharge was independently associated with increased all-cause mortality (HR per 1 kPa increase 1.098, 95% CI 1.025-1.176, p=0.008), higher risk of HF hospitalization (HR 1.075, 95% CI 1.035-1.117, p.

Carotid body size on CTA: correlation with comorbidities.

AIM: To test the hypothesis that computed tomographic angiography (CTA) can identify carotid body enlargement in patients with sympathetically mediated diseases. MATERIALS AND METHODS: A retrospective chart review of all patients obtaining CTAs of the cervical vasculature at University of Utah Health Sciences Center over a 6-month period was performed. Widest axial measurements of both carotid bodies were performed on a picture archiving and communication system (PACS). Statistical analysis was then performed to compare the mean carotid body size between control patients and patients with diabetes mellitus, hypertension, and congestive heart failure. RESULTS: Measurements were performed on 288 patients, with 134 controls. Of the remaining 154, 72 patients had diabetes mellitus, 46 had congestive heart failure, and 130 had hypertension. The control patients had a mean carotid body diameter of 2.3 mm. There was a statistically significant (p < 0.01) 20-25% increase in mean diameter with diabetes mellitus (2.8 mm), hypertension (2.7 mm), and congestive heart failure (2.7 mm; p < 0.01). CONCLUSIONS: This study found a 20-25% larger mean carotid body size in patients with diabetes mellitus, hypertension, and congestive heart failure relative to controls. However, this small enlargement should not mimic other carotid body diseases, such as a paraganglionoma. Moreover, these findings further support the proposed functional relationship between the carotid body and sympathetically mediated disease states.

Reversible cardiomyopathies--a review.

End-stage renal disease, cirrhosis, obesity, tachycardia, and extreme stress have all been shown to result in impaired left ventricular function. It is becoming clear, however, that the cardiomyopathies associated with these states are reversible after resolution of the underlying process. In this article, we present the current data demonstrating that renal transplantation, liver transplantation, and bariatric surgery can lead to reversal of uremic, cirrhotic, and obesity cardiomyopathies, respectively. We also discuss the reversibility of tachycardia-induced cardiomyopathy after radiofrequency ablation or pharmacologic therapy for rate or rhythm control and the reversibility of stress-induced cardiomyopathy with supportive care.