Molecular mechanisms in evolutionary cardiology failure

Area of Science:

• Evolutionary biology
• Cardiology
• Molecular medicine

Background:

• Historically, heart failure (HF) was attributed to infections, and cardiac hypertrophy (CH) to mechanical stress.
• Modern lifestyles have decreased infections and increased lifespan, shifting HF's understanding to a complex interplay of mechanical disorder, ischemia, and senescence.
• Myocardial fibrosis significantly impacts diastolic function and arrhythmias, posing a major challenge in HF management.

Purpose of the Study:

• To integrate the evolutionary paradigm into understanding heart failure (HF) and cardiac hypertrophy (CH).
• To highlight the adaptive nature of cardiac hypertrophy (CH) as a physiological response to pathological stimuli.
• To emphasize the evolving therapeutic goals for HF, focusing on economic rather than inotropic interventions.

Main Methods:

• Review of historical and recent literature on heart failure (HF) and cardiac hypertrophy (CH).
• Analysis of the impact of lifestyle changes on cardiovascular disease prevalence and presentation.
• Integration of findings from microRNA research to understand fetal gene reprogramming in cardiac hypertrophy (CH).

Main Results:

• Cardiac hypertrophy (CH) is confirmed as a valid adaptive process aimed at restoring myocardial economy.
• Fetal gene reprogramming, both quantitative and qualitative, characterizes the adaptive response in CH, supported by microRNA research.
• Recent lifestyle changes have significantly altered the context and presentation of HF.

Conclusions:

• Cardiac hypertrophy (CH) represents a physiological reaction to a pathological stimulus, driven by adaptive mechanisms.
• Therapeutic strategies for HF should prioritize economic restoration over inotropic support.
• Understanding the evolutionary context and molecular underpinnings of HF is crucial for effective management.