Three left ventricular leads required for improved haemodynamic and clinical status of a patient with very severe heart failure and a narrow QRS duration

Objective. To compare the effect of torasemide (Td) and furosemide (Fd) on the daily blood pressure profile (DBPP), blood pressure (BP) during aclive orthostatic test (OT) and dynamics in brain natriuretic peptide (BNP) levels in patients with heart failure (HF) III-IV (NYHA). Design and methods. 40 patients with stable HF III-IV (NYHA); left ventricular ejection fraction (LVEF) ≤ 40 %; 90 ≤ systolic BP ≤ 140 mmHg; 60 ≤ diastolic BP ≤ 90 mmHg were included. Clinical status, 6-minute walking test (SWT), BNP and aldosterone levels, quality of live (QL), DBPP, OT were assessed. The patients were randomized into two groups: torasemide group TG (n = 20) receiving Td, and furosemide group (FG) (n = 20) receiving Fd. Results. The patients with lower BP during OT and DBPP had higher level of BNP. The low BP levels complicated with drug titration till the recommended doses for HF reatment. We observed the decrease of HF functional class, BNP level, the increased distance in SWT in both groups. TG showed higher BP levels and less BP decrease during OT that allowed us to achieve the highest β-blockers doses and significantly improve QL. Conclusions. 1. Patients with HF with lower BP during DBPP and more expressed decrease of BP in OT had a higher BNP level. 2. The Fd replacement by Td results in the decrease of orthostatic reaction, optimization of SBPP and more significant positive changes in QL. 3. The replacement Fd by Td allows significantly increasing the doses of β-blockers.

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Echocardiographic assessment of the effects of acute left ventricular pacing on patients with severe congestive heart failure and narrow QRS duration

Critical Care ◽

10.1186/cc7319 ◽

2009 ◽

Vol 13 (Suppl 1) ◽

pp. P155

Author(s):

K Hussein ◽

H Elaassar ◽

D Ragab ◽

H Elattroush ◽

R Soliman ◽

...

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Severe Congestive Heart Failure ◽

Left Ventricular ◽

Ventricular Pacing ◽

Narrow Qrs ◽

Qrs Duration ◽

Left Ventricular Pacing ◽

Echocardiographic Assessment

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Left Ventricular Septolateral Mechanical Delay Is Associated with Reduced Long-Term Survival in Systolic Heart Failure with Narrow QRS Duration: Nine-Year Outcome in 109 Patients

Echocardiography ◽

10.1111/echo.12904 ◽

2015 ◽

Vol 32 (10) ◽

pp. 1515-1519

Author(s):

Srikanth Krishnan ◽

Sanjay Verma ◽

Michael Cheng ◽

Rajagopal Krishnan ◽

Ramdas G. Pai

Keyword(s):

Heart Failure ◽

Systolic Heart Failure ◽

Left Ventricular ◽

Term Survival ◽

Long Term Survival ◽

Narrow Qrs ◽

Qrs Duration

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P2126 Intrinsic and paced QRS duration are predictive of the global clinical response to cardiac resynchronization therapy in patients with severe heart failure

European Heart Journal ◽

10.1016/s0195-668x(03)95120-7 ◽

2003 ◽

Vol 24 (5) ◽

pp. 397

Author(s):

G LECOQ

Keyword(s):

Heart Failure ◽

Cardiac Resynchronization Therapy ◽

Clinical Response ◽

Severe Heart Failure ◽

Cardiac Resynchronization ◽

Resynchronization Therapy ◽

Qrs Duration

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Cardiac mitofusin-1 is declined in non-responding patients with idiopathic dilated cardiomyopathy

European Heart Journal ◽

10.1093/ehjci/ehaa946.3601 ◽

2020 ◽

Vol 41 (Supplement_2) ◽

Author(s):

Y Hsiao ◽

I Shimizu ◽

T Wakasugi ◽

S Jiao ◽

T Watanabe ◽

...

Keyword(s):

Electron Microscopy ◽

Heart Failure ◽

Ventricular Myocytes ◽

Severe Heart Failure ◽

Left Ventricular ◽

Neonatal Rat ◽

Heart Failure Patients ◽

Underlying Mechanisms ◽

Neonatal Rat Ventricular Myocytes ◽

Mitofusin 1

Abstract Background/Introduction Mitochondria are dynamic regulators of cellular metabolism and homeostasis. The dysfunction of mitochondria has long been considered a major contributor to aging and age-related diseases. The prognosis of severe heart failure is still unacceptably poor and it is urgent to establish new therapies for this critical condition. Some patients with heart failure do not respond to established multidisciplinary treatment and they are classified as “non-responders”. The outcome is especially poor for non-responders, and underlying mechanisms are largely unknown. Purpose Studies indicate mitochondrial dysfunction has causal roles for metabolic remodeling in the failing heart, but underlying mechanisms remain to be explored. This study tried to elucidate the role of Mitofusin-1 in a failing heart. Methods We examined twenty-two heart failure patients who underwent endomyocardial biopsy of intraventricular septum. Patients were classified as non-responders when their left-ventricular (LV) ejection fraction did not show more than 10% improvement at remote phase after biopsy. Fourteen patients were classified as responders, and eight as non-responders. Electron microscopy, quantitative PCR, and immunofluorescence studies were performed to explore the biological processes or molecules involved in failure to respond. In addition to studies with cardiac tissue specific knockout mice, we also conducted functional in-vitro studies with neonatal rat ventricular myocytes. Results Twenty-two patients with IDCM who underwent endomyocardial biopsy were enrolled in this study, including 14 responders and 8 non-responders. Transmission electron microscopy (EM) showed a significant reduction in mitochondrial size in cardiomyocytes of non-responders compared to responders. Quantitative PCR revealed that transcript of mitochondrial fusion protein, Mitofusin-1, was significantly reduced in non-responders. Studies with neonatal rat ventricular myocytes (NRVMs) indicated that the beta-1 adrenergic receptor-mediated signaling pathway negatively regulates Mitofusin-1 expression. Suppression of Mitofusin-1 resulted in a significant reduction in mitochondrial respiration of NRVMs. We generated left ventricular pressure overload model with thoracic aortic constriction (TAC) in cardiac specific Mitofusin-1 knockout model (c-Mfn1 KO). Systolic function was reduced in c-Mfn1 KO mice, and EM study showed an increase in dysfunctional mitochondria in the KO group subjected to TAC. Conclusions Mitofusin-1 becomes a biomarker for non-responders with heart failure. In addition, our results suggest that therapies targeting mitochondrial dynamics and homeostasis would become next generation therapy for severe heart failure patients. Funding Acknowledgement Type of funding source: None

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Anaemia and heart failure

Open Medicine ◽

10.2478/s11536-010-0060-3 ◽

2011 ◽

Vol 6 (1) ◽

pp. 11-25

Author(s):

Enrico Vizzardi ◽

Tania Bordonali ◽

Elena Tanghetti ◽

Marco Metra ◽

Livio Cas

Keyword(s):

Heart Failure ◽

Ventricular Dysfunction ◽

Severe Heart Failure ◽

Left Ventricular ◽

Favourable Effect ◽

Heart Failure Trial ◽

Patients With Heart Failure ◽

Darbepoetin Alpha ◽

Main Determinants ◽

Independent Determinant

AbstractAnaemia is one of the most frequent co-morbidities in patients with heart failure. Its prevalence increases from 4% to7% in subjects with asymptomatic left ventricular dysfunction to >30% in patients with severe heart failure. Renal insufficiency, activation of inflammatory mediators and treatment with renin-angiotensin antagonists seem to be its main determinants. The results of many studies agree in providing evidence that anaemia is a powerful independent determinant of survival in patients with heart failure. However, the mechanisms of this relation are still not fully understood. Moreover a favourable effect of the correction of anaemia on prognosis has not yet been shown. Also In addition to this, controlled studies assessing its effects on exercise tolerance have yielded controversial results. Further research is needed to assess the effect of correcting anaemia in chronic heart failure (CHF) patients; ongoing reduction of events with RED-HF (Darbepoetin alpha in heart failure) trial will help define the role.

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