Congestive heart failure with preserved EF
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]
Overview
LV remodeling is the basic concept for HFpEF pathophysiolgy. Two models are emerging in HFpEF pathophysiology, the traditional model discussed about ventricular diastolic dysfunction , LV hypertrophy, impaired relaxation, endothelial dysfunction, arterial and ventricular stiffness and their effect on cardiac function. The emerged model discussed role of systemic microvascular endothelial inflammation due to existing comorbidities such as, diabetes, hypertension, obesity, smoking and ischemia in cardiac remodeling and dysfunction.
Pathophysiology
Traditional Model
Traditionally, it is believed that fundamental pathophysiology of heart failure with preserved ejection fraction (HFpEF) is related to hypertensive left ventricular remodeling.[1] Factors contributing to this feature include
Ventricular diastolic dysfunction
Diastolic dysfunction is the main stay in developing heart failure with preserved EF (HFpEF). Patients with HFpEF have more impaired LV relaxation and diastolic stiffness compared to healthy or hypertensive controls without heart failure.[2][3]
However, severity of hypertrophy does not distinguish between hypertensive patients with and without heart failure.[4]
LV hypertrophy
LV mass is higher in patients with HFpEF comparing to healthy people or hypertensive patients.[5]
Slow relaxation
Cardiac relaxation depends on calcium reuptake and elastic properties of myocardium. In the presence of tachycardia, it may result in increasing in LV filling pressure.[6]
Endothelial dysfunction
Systemic vasorelaxation in response to exercise is attenuated in HFpEF due to impaired endothelial function.[7][8]
Arterial and ventricular stiffening
Both arterial stiffness and LV systolic stiffness are increased in hypertensive patients and patients with HFpEF.[9][3]
Emerging Model
This is the new model describing the pathophysilogic feature of HFpEF. The most important Contributing factor in this model is systemic microvascular endothelial inflammation that may result in cardiac remodeling and dysfunction.
Systemic microvascular endothelial inflammation
This endothelial inflammation is due to underlying coexisting condition such as, hypertension, obesity, ischemia, diabetes, the metabolic syndrome, lung disease, smoking, and iron deficiency.[10]
| Increases in oxidative stress, Decreases in NO–cyclic GMP signaling | Myofiber stiffness, Cardiomyocyte hypertrophy | ||||||||||||||||||||||||||||||||||||||||||||||
| Systemic microvascular endothelial inflammation | Muscle inflammation | Fibrosis | Global cardiac remodeling and dysfunction Impaired coronary flow reserve Impaired oxygen delivery, uptake, and utilization in skeletal muscle | ||||||||||||||||||||||||||||||||||||||||||||
| Microvascular dysfunction and rarefaction | |||||||||||||||||||||||||||||||||||||||||||||||
Coronary microvascular inflammation
Coronary microvascular inflammation may results in microvascular dysfunction and rarefaction with reduced microvascular density and coronary flow reserve.[10] Similar changes may result in systemic muscular dysfunction.
References
- ↑ Gladden JD, Linke WA, Redfield MM (2014). “Heart failure with preserved ejection fraction”. Pflugers Arch. 466 (6): 1037–53. doi:10.1007/s00424-014-1480-8. PMC 4075067. PMID 24663384.
- ↑ Borlaug BA, Jaber WA, Ommen SR, Lam CS, Redfield MM, Nishimura RA (2011). “Diastolic relaxation and compliance reserve during dynamic exercise in heart failure with preserved ejection fraction”. Heart. 97 (12): 964–9. doi:10.1136/hrt.2010.212787. PMC 3767403. PMID 21478380.
- ↑ 3.0 3.1 Lam CS, Roger VL, Rodeheffer RJ, Bursi F, Borlaug BA, Ommen SR, Kass DA, Redfield MM (2007). “Cardiac structure and ventricular-vascular function in persons with heart failure and preserved ejection fraction from Olmsted County, Minnesota”. Circulation. 115 (15): 1982–90. doi:10.1161/CIRCULATIONAHA.106.659763. PMC 2001291. PMID 17404159.
- ↑ Lam CS, Roger VL, Rodeheffer RJ, Borlaug BA, Enders FT, Redfield MM (2009). “Pulmonary hypertension in heart failure with preserved ejection fraction: a community-based study”. J. Am. Coll. Cardiol. 53 (13): 1119–26. doi:10.1016/j.jacc.2008.11.051. PMC 2736110. PMID 19324256.
- ↑ Mohammed SF, Borlaug BA, Roger VL, Mirzoyev SA, Rodeheffer RJ, Chirinos JA, Redfield MM (2012). “Comorbidity and ventricular and vascular structure and function in heart failure with preserved ejection fraction: a community-based study”. Circ Heart Fail. 5 (6): 710–9. doi:10.1161/CIRCHEARTFAILURE.112.968594. PMC 3767407. PMID 23076838.
- ↑ Phan TT, Abozguia K, Nallur Shivu G, Mahadevan G, Ahmed I, Williams L, Dwivedi G, Patel K, Steendijk P, Ashrafian H, Henning A, Frenneaux M (2009). “Heart failure with preserved ejection fraction is characterized by dynamic impairment of active relaxation and contraction of the left ventricle on exercise and associated with myocardial energy deficiency”. J. Am. Coll. Cardiol. 54 (5): 402–9. doi:10.1016/j.jacc.2009.05.012. PMID 19628114.
- ↑ Borlaug BA, Melenovsky V, Russell SD, Kessler K, Pacak K, Becker LC, Kass DA (2006). “Impaired chronotropic and vasodilator reserves limit exercise capacity in patients with heart failure and a preserved ejection fraction”. Circulation. 114 (20): 2138–47. doi:10.1161/CIRCULATIONAHA.106.632745. PMID 17088459.
- ↑ Borlaug BA, Olson TP, Lam CS, Flood KS, Lerman A, Johnson BD, Redfield MM (2010). “Global cardiovascular reserve dysfunction in heart failure with preserved ejection fraction”. J. Am. Coll. Cardiol. 56 (11): 845–54. doi:10.1016/j.jacc.2010.03.077. PMC 2950645. PMID 20813282.
- ↑ Borlaug BA, Lam CS, Roger VL, Rodeheffer RJ, Redfield MM (2009). “Contractility and ventricular systolic stiffening in hypertensive heart disease insights into the pathogenesis of heart failure with preserved ejection fraction”. J. Am. Coll. Cardiol. 54 (5): 410–8. doi:10.1016/j.jacc.2009.05.013. PMC 2753478. PMID 19628115.
- ↑ 10.0 10.1 Redfield, M. M., et al. “Heart Failure with Preserved Ejection Fraction.” N Engl J Med 2016.375 (2016): 1868-1877.
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