Patient-Centered Heart Failure Therapy Samson, Rohan; Ennezat, Pierre V; Jemtel, Thierry H Le
The American journal of medicine
137, Številka:
1
Journal Article
Recenzirano
Simultaneous initiation of quadruple therapy with angiotensin receptor-neprilysin inhibitor, beta-adrenergic receptor blocker, mineralocorticoid receptor antagonist, and sodium glucose cotransporter ...2 inhibitor aims at prompt improvement and prevention of readmission in patients hospitalized for heart failure with reduced ejection fraction. However, titration of quadruple therapy is time consuming. Lengthy up-titration of quadruple therapy may negate the benefit of early initiation. Quadruple therapy should start with a sodium glucose cotransporter 2 inhibition and a mineralocorticoid antagonist, as both enable safe decongestion and require minimal or no titration. Depending on the level of decongestion and clinical characteristics, patients receive an angiotensin receptor-neprilysin inhibitor or a beta-adrenergic receptor blocker to be titrated after hospital discharge. Outpatient addition of an angiotensin receptor-neprilysin inhibitor to a beta-adrenergic receptor blocker or vice versa completes the quadruple therapy scheme. By focusing on decongestion and matching intervention to patients' profile, the present therapeutic sequence allows rapid implementation of quadruple therapy at fully recommended doses.
Purpose of Review
Epicardial adipose tissue has been associated with the development/progression of cardiovascular disease. We appraise the strength of the association between epicardial adipose ...tissue and development/progression of cardiovascular diseases like coronary artery disease, atrial fibrillation, and heart failure with preserved ejection fraction.
Recent Findings
Cross-sectional clinical and translational correlative studies have established an association between epicardial adipose tissue and progression of coronary artery disease. Recent studies question this association and underline the need for longitudinal studies. Epicardial adipose tissue also plays a definite role in the pathobiology of atrial fibrillation and its recurrence after ablation. In contrast to an early paradigm, epicardial adipose tissue does not appear to play a key role in the pathogenesis of heart failure with preserved ejection fraction in obese patients.
Summary
The association of epicardial adipose tissue with atrial fibrillation is robust. In contrast, the association of epicardial adipose tissue with coronary artery disease and heart failure with preserved ejection fraction is tenuous. Additional research, including longitudinal studies, is needed to confirm or refute these proposed associations.
Abstract The findings of randomized trials of neurohormonal modulation have been neutral in heart failure with preserved ejection fraction and consistently positive in heart failure with reduced ...ejection. Left ventricular remodeling promotes the development and progression of heart failure with preserved and reduced ejection fraction. However, different stimuli mediate left ventricular remodeling that is commonly concentric in heart failure with preserved ejection fraction and eccentric in heart failure with reduced ejection. The stimuli that promote concentric left ventricular remodeling may account for the neutral findings of neuhormonal modulation in heart failure with preserved ejection fraction. Low‐grade systemic inflammation‐induced microvascular endothelial dysfunction is currently the leading hypothesis behind the development and progression of heart failure with preserved ejection fraction. The hypothesis provided the rationale for several randomized controlled trials that have led to neutral findings. The trials and their limitations are reviewed.
Background
Bariatric surgery may improve heart failure outcome in morbidly obese patients. However, the safety of bariatric surgery has not been investigated in morbidly obese patients hospitalized ...for heart failure. We evaluated the effects of bariatric surgery on parameters of hospitalization for heart failure in morbidly obese patients.
Methods
We analyzed administrative discharge data of morbidly obese patients with heart failure as a primary diagnosis. Propensity score matching was performed to assess parameters of hospitalization in morbidly obese patients with and without a history of bariatric surgery. The discharges with diastolic heart failure codes were analyzed separately.
Results
Morbid obesity was coded in 4.4% of all discharges. Heart failure was the primary diagnosis in 6.0% of discharges with morbid obesity codes. Only 1% of discharges with morbid obesity and heart failure as primary diagnosis codes were coded for bariatric surgery. Length of stay (
p
< 0.001), in-hospital mortality (
p
< 0.001), and the estimated cost of hospitalizations (
p
< 0.007) were lower in discharges with than without bariatric surgery codes. Length of stay was shorter and in-hospital mortality was lower in discharges with codes for diastolic heart failure and bariatric surgery than with codes for only diastolic heart failure (
p
< 0.042 and
p
< 0.001 respectively).
Conclusion
When hospitalized for heart failure, morbidly obese patients who underwent bariatric surgery fare as well as or slightly better than their counterparts who did not.
Unrecognized obstructive sleep apnea (OSA) is highly prevalent in obesity. Both obesity and OSA are associated with vascular endothelial inflammation and increased risk for cardiovascular diseases. ...We investigated directly whether the endothelial alterations that are attributed commonly to obesity are in fact related to OSA.
Seventy-one subjects with a body mass index ranging from normal to obese underwent attended polysomnography. To assess vascular inflammation and oxidative stress directly, we quantified the expression of nuclear factor-kappaB and nitrotyrosine by immunofluorescence in freshly harvested venous endothelial cells. To evaluate basal endothelial nitric oxide (NO) production and activity, we quantified the expression of endothelial NO synthase (eNOS) and phosphorylated eNOS. Vascular reactivity was measured by brachial artery flow-mediated dilation. Expression of eNOS and phosphorylated eNOS and flow-mediated dilation were significantly lower, whereas expression of nitrotyrosine was significantly greater in OSA patients (n=38) than in OSA-free subjects (n=33) regardless of central adiposity. Expression of nuclear factor-kappaB was greater in obese OSA patients than in obese OSA-free subjects (P=0.004). Protein expression and flow-mediated dilation were not significantly affected by increasing body mass index or central obesity in OSA patients and in OSA-free subjects. After 4 weeks of continuous positive airway pressure therapy, flow-mediated dilation and expression of eNOS and phosphorylated eNOS significantly increased whereas expression of nitrotyrosine and nuclear factor-kappaB significantly decreased in OSA patients who adhered to continuous positive airway pressure >/=4 hours daily.
Untreated OSA rather than obesity is a major determinant of vascular endothelial dysfunction, inflammation, and elevated oxidative stress in obese patients.
Purpose of Review
Anti-hypertensive and lipid lowering therapy addresses only half of the cardiovascular disease risk in patients with body mass index > 30 kg/m
2
, i.e., obesity. We examine newer ...aspects of obesity pathobiology that underlie the partial effectiveness of anti-hypertensive lipid lowering therapy for the reduction of cardiovascular disease risk in obesity.
Recent Findings
Obesity-related insulin resistance, vascular endothelium dysfunction, increased sympathetic nervous system/renin–angiotensin–aldosterone system activity, and glomerulopathy lead to type 2 diabetes, coronary atherosclerosis, and chronic disease kidney disease that besides hypertension and dyslipidemia increase cardiovascular disease risk.
Summary
Obesity increases cardiovascular disease risk through multiple pathways. Optimal reduction of cardiovascular disease risk in patients with obesity is likely to require therapy targeted at both obesity and obesity-associated conditions.
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