Chronic Heart Failure Clinical Practice Guidelines' Class 1-A Pharmacologic Recommendations: Start-to-End Synergistic Drug Therapy?

BACKGROUND: Chronic heart failure (HF) disease as an emerging epidemic has a high economic-psycho-social burden, hospitalization, readmission, morbidity and mortality rates despite many clinical practice guidelines' evidenced-based and consensus driven recommendations that include trials' initial-baseline data. OBJECTIVE: To show that the survival and hospitalization-free event rates in the reviewed chronic HF clinical practice guidelines' class I-A recommendations as initial HF drug therapy (IDT) is possibly a combination and 'start-to-end' synergistic effect of the add-on ('end') HF drug therapy (ADT) to the baseline ('start') HF drug therapy (BDT). METHODOLOGY: The references cited in the chronic HF clinical practice guidelines of the 2005, 2009, and 2013 American Heart Association/American College of Cardiology (AHA/ACC), the 2006 Heart Failure Society of America (HFSA), and the 2005, 2008, and 2012 European Society of Cardiology (ESC) were reviewed and compared with the respective guidelines' and other countries' recommendations. RESULTS: The BDT using glycosides and diuretics is 79%-100% in the cited HF trials. The survival rates attributed to the BDT ('start') is 46%-89% and IDT ('end') 61%-92.8%, respectively. The hospitalization-free event rate of the BDT group: 47.1% to 85.3% and IDT group 61.8%-90%, respectively. Thus, the survival and hospitalization-free event rates of the ADT is 0.4%-15% and 4.6% to 14.7%, respectively. The extrapolated BDT survival is 8%-51% based on a 38% estimated natural HF survival rate for the time period109. CONCLUSION: The contribution of baseline HF drug therapy (BDT) is relevant in terms of survival and hospitalization-free event rates compared to the HF class 1-A guidelines initial drug therapy recommendations (IDT). Further, the proposed initial HF drug ('end') therapy (IDT) has possible synergistic effects with the baseline HF drug ('start') therapy (BDT) and is essentially the add on HF drug therapy (ADT) in our analysis. The polypharmacy HF treatment is a synergistic effect due to BDT and ADT.

Chronic heart failure guidelines: A critique

BACKGROUND: Chronic heart failure (HF) disease as an emerging epidemic has a high economic burden, hospitalization, readmission, morbidity rates despite many clinical practice guidelines recommendations. OBJECTIVE: To show that the attributed survival and hospitalization-free event rates in the reviewed chronic HF clinical practice guidelines' Class I-A recommendations as "initial HF drug therapy" is basically "add-on HF drug therapy" to the "baseline HF drug therapy" thereby under-estimating the "baseline HF drug therapy" significant contribution to the clinical outcome. METHODOLOGY: The references cited in the chronic HF clinical practice guidelines of the American Heart Association/American College of Cardiology (AHA/ACC), the Heart Failure Society of America (HFSA), and the European Society of Cardiology (ESC) were reviewed and compared with the respective guidelines' and other countries' recommendations. RESULTS: The "baseline HF drug therapy" using glycosides and diuretics is 79-100% in the cited HF trials. The survival and hospitalization event-free rates attributed to the "baseline HF drug therapy" are 46-89% and 61.8-90%, respectively. The survival and hospitalization-free event rate of the "initial HF drug therapy" is 61-92.8% and 61.8-90%, respectively. Thus the survival and hospitalization event-free rates of the "add-on HF drug therapy" are 0.4-15% and 4.6% to 14.7%, respectively. The extrapolated "baseline HF drug therapy" survival is 8-51% based on a 38% natural HF survival rate for the time period. CONCLUSION: The contribution of "baseline HF drug therapy" is relevant in terms of survival and hospitalization event-free rates compared to the HF Class 1-A guidelines proposed "initial HF drug therapy" which is in essence an "add-on HF drug therapy" in this analysis.

A plump and fatty heart: isolated left ventricular apical hypoplasia.

Isolated left ventricular apical hypoplasia is a newly recognized type of cardiomyopathy, with only a few cases reported since it was first described in 2004. We report this case of a 21-year-old Filipino female presenting with unstable supraventricular arrhythmia and heart failure, with characteristic features of isolated left ventricular apical hypoplasia on echocardiography and cardiac magnetic resonance imaging. To our knowledge, this is the first reported adult case in Asia.

Microcirculation: target therapy in cardiovascular diseases - a clinical perspective.

Microcirculation conduit, distribution, exchange and reception vessels usually retain a demand-dependent vascular-tissue match as well as a nutrient friendly capillary-matrix tissue match. Various stimuli can initiate a vascular-capillary matrix-tissue mismatch. Counter-regulatory mechanisms result in hyperplasia or apoptosis. Microvascular disease (MVD) as a consequence or outcome of supply-demand mismatch has clinical therapeutic and prognostic implications in the hypertensive syndrome and coronary artery disease (CAD) cases. Recognition of the role of apoptosis and MVD may initiate a paradigm shift in clinical practice. Digitalis and other anti-hypertensive agents have anti-apoptotic action and MVD blunting effects that can control LVH development to reduce congestive heart failure (CHF) progression.

Microvascular disease relevance in the hypertension syndrome.

Hypertension is not an isolated problem. Co-morbidities of smoking, obesity, diabetes and dyslipidemia are all associated with microvascular disease (MVD) with abnormal PET scan and endothelial dysfunction. MVD may contribute to left ventricular hypertrophy (LVH) via an imbalance between hyperplasia and apoptotic signals. Digitalis and other anti-hypertensive agents have anti-apoptotic action and MVD blunting effects, respectively. Heart failure progression must then be based on the preservation of myocyte integrity. Indeed, altered contractility appears to be a consequence of rather than the cause of myocyte deterioration. LV systolic dysfunction improvement is already a late strategy. Furthermore, the efficacy of anti-hypertension therapy may be limited in restoring LV diastolic function. Recognition of the role of apoptosis and MVD may initiate a paradigm shift in clinical practice.