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Congestive Heart Failure

last updated: June 3, 2016

Congestive Heart Failure

Heart Failure



Heart not strong enough, either from a structural or functional impairment of ventricular filling (diastolic dysfunction) or poor ejection of blood (systolic dysfunction), to meet the metabolic demands of the body.



  •  > 20 million people affected worldwide

  • Adult Prevalence in developed countries is 2%.

  • Heart Failure prevalence follows an exponential pattern, rising with age, and affects 6–10% of people over age 65.

  • Relative incidence of heart failure is lower in women than in men, women constitute at least one-half the cases probably because of their longer life expectancy.

  • In North America and Europe, the lifetime risk of developing heart failure is approximately 1 in 5 for a 40-year-old.


The overall prevalence of heart failure is thought to be increasing, partly because current therapies for cardiac disorders, such as myocardial infarction (MI), valvular heart disease, and arrhythmias, are allowing patients to survive longer.


Very little is known about the prevalence or risk of developing heart failure in emerging nations because of the lack of population-based studies in those countries.

  • Rheumatic heart disease remains a major cause in Africa and Asia, especially in the young.

  • Hypertension in the African and African American populations

  • Chagas’ disease in South America

  • Not surprisingly, anemia is a frequent concomitant factor in heart failure in many developing nations.

  • As developing nations undergo socioeconomic development, the epidemiology of heart failure is becoming similar to that of Western Europe and North America, with CAD emerging as the single most common cause of heart failure.

  • Although the contribution of diabetes mellitus to heart failure is not well understood, diabetes accelerates atherosclerosis and often is associated with hypertension (Harrison's).


Pathophysiology (input/output problem)

If you look at the heart it acts like a pump with blood going in and out of it. In heart failure, there is not enough blood going out of the heart or not enough blood going into the heart thus producing the two major signs:

  • poor end organ perfusion and/or

  • congestion because not enough blood going into the heart and thus backup occurs.


It is these two major signs that classify heart failure as either having systolic or diastolic dysfunction.


Regardless of the dysfunction, a fall in cardiac output activates several compensatory mechanisms via the baroreceptors:

  • low kidney blood flow activates the renin-angiotensin-aldosterone (RAA) system

  • sympathetic nervous system

  • ADH system

  • various countervailing vasodilatory molecules, including the atrial and brain natriuretic peptides (ANP and BNP), prostaglandins (PGE2 and PGI2), and nitric oxide (NO), that offsets the excessive peripheral vascular vasoconstriction


These compensatory pathways are aimed to maintain cardiac output. Vasoconstriction and fluid retention cause the heart to pump harder and so it compensates for its dead cells by enlarging which now holds less volume (EDV). This will cause lower cardiac output, the cycle continues and eventually if this process is left unhalted it can lead to vicious cycles and worsening of heart failure and eventual death.  


Genetic background, sex, age, or environment may influence these compensatory mechanisms, which are able to modulate LV function within a physiologic/homeostatic range so that the functional capacity of the patient is preserved or is depressed only minimally.


Patients may remain asymptomatic or minimally symptomatic for a period of years; however, at some point patients become overtly symptomatic, with a resultant striking increase in morbidity and mortality. Although the exact mechanisms that are responsible for this transition are not known, the transition to symptomatic heart failure is accompanied by increasing activation of neurohormonal, adrenergic, and cytokine systems that lead to a series of adaptive changes within the myocardium collectively referred to as left ventricular (LV) remodeling.


LV Remodeling

- an adaptive change the heart undergoes after cardiac injury and/or abnormal hemodynamic loading conditions

- refers to the changes in size, shape, and function of the heart 

- occurs when the following biological stimuli are present:

  • mechanical stretch of the myocyte

  • circulating neurohormones (e.g. norepinephrine, angiotensin II)

  • inflammatory cytokines (e.g., tumor necrosis factor [TNF])

  • other peptides and growth factors (e.g., endothelin)

  • reactive oxygen species (e.g., superoxide)

- LV remodeling may contribute independently to the progression of heart failure by virtue of the mechanical burdens that are engendered by the changes in the geometry of the remodeled LV


LV remodeling develops in response to these stimuli and develops a series of complex events that occur at the cellular and molecular levels. These changes include:

  1. myocyte hypertrophy

  2. alterations in the contractile properties of the myocyte

  3. progressive loss of myocytes through necrosis, apoptosis, and autophagic cell death

  4. β-adrenergic desensitization

  5. abnormal myocardial energetics and metabolism

  6. reorganization of the extracellular matrix with dissolution of the organized structural collagen weave surrounding myocytes and subsequent replacement by an interstitial collagen matrix that does not provide structural support to the myocytes.


The sustained overexpression of these biologically active molecules is believed to contribute to the progression of heart failure by virtue of the deleterious effects they exert on the heart and the circulation. Indeed, this insight forms the clinical rationale for using pharmacologic agents that antagonize these systems (e.g., angiotensin-converting enzyme [ACE] inhibitors and beta blockers) in treating patients with heart failure.


In addition to the increase in LV end-diastolic volume, LV wall thinning occurs as the left ventricle begins to dilate. The increase in wall thinning, along with the increase in afterload created by LV dilation, leads to a functional afterload mismatch that may contribute further to a decrease in stroke volume. Moreover, the high end-diastolic wall stress might be expected to lead to

(1) hypoperfusion of the subendocardium, with resultant worsening of LV function;

(2) increased oxidative stress, with the resultant activation of families of genes that are sensitive to free radical generation (e.g., TNF and interleukin 1β); and

(3) sustained expression of stretch-activated genes (angiotensin II, endothelin, and TNF) and/or stretch activation of hypertrophic signaling pathways.


Increasing LV dilation also results in tethering of the papillary muscles with resulting incompetence of the mitral valve apparatus and functional mitral regurgitation, which in turn leads to further hemodynamic overloading of the ventricle. Taken together, the mechanical burdens that are engendered by LV remodeling contribute to the progression of heart failure.


Recent studies have shown that LV remodeling can be reversed following medical and device therapy and that reverse LV remodeling is associated with improved clinical outcomes in patients with heart failurer. Indeed, one of the goals of therapy for heart failure is to prevent and/or reverse LV remodeling.


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