Congestive heart failure with preserved EF

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Congestive Heart Failure Microchapters


Patient Information


Historical Perspective



Systolic Dysfunction
Diastolic Dysfunction


Differentiating Congestive heart failure from other Diseases

Epidemiology and Demographics

Risk Factors


Natural History, Complications and Prognosis


Clinical Assessment

History and Symptoms

Physical Examination

Laboratory Findings


Chest X Ray

Cardiac MRI


Exercise Stress Test

Myocardial Viability Studies

Cardiac Catheterization

Other Imaging Studies

Other Diagnostic Studies


Invasive Hemodynamic Monitoring

Medical Therapy:

Acute Pharmacotherapy
Chronic Pharmacotherapy in HFpEF
Chronic Pharmacotherapy in HFrEF
ACE Inhibitors
Angiotensin receptor blockers
Aldosterone Antagonists
Beta Blockers
Ca Channel Blockers
Positive Inotropics
Angiotensin Receptor-Neprilysin Inhibitor
Antiarrhythmic Drugs
Nutritional Supplements
Hormonal Therapies
Drugs to Avoid
Drug Interactions
Treatment of underlying causes
Associated conditions

Exercise Training

Surgical Therapy:

Biventricular Pacing or Cardiac Resynchronization Therapy (CRT)
Implantation of Intracardiac Defibrillator
Cardiac Surgery
Left Ventricular Assist Devices (LVADs)
Cardiac Transplantation

ACC/AHA Guideline Recommendations

Initial and Serial Evaluation of the HF Patient
Hospitalized Patient
Patients With a Prior MI
Sudden Cardiac Death Prevention
Surgical/Percutaneous/Transcather Interventional Treatments of HF
Patients at high risk for developing heart failure (Stage A)
Patients with cardiac structural abnormalities or remodeling who have not developed heart failure symptoms (Stage B)
Patients with current or prior symptoms of heart failure (Stage C)
Patients with refractory end-stage heart failure (Stage D)
Coordinating Care for Patients With Chronic HF
Quality Metrics/Performance Measures

Implementation of Practice Guidelines

Congestive heart failure end-of-life considerations

Specific Groups:

Special Populations
Patients who have concomitant disorders
Obstructive Sleep Apnea in the Patient with CHF
NSTEMI with Heart Failure and Cardiogenic Shock

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]


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.


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
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.


  1. 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.
  2. 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. 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.
  4. 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.
  5. 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.
  6. 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.
  7. 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.
  8. 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.
  9. 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. 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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