What complications can result from heart valve dysfunction, specifically: sudden cardiac death, heart failure, or decreased ejection fraction?

Heart Valve Dysfunction Complications

All of these complications—sudden cardiac death, heart failure, and decreased ejection fraction—can result from heart valve dysfunction. 1

Comprehensive Complication Profile

Heart valve dysfunction leads to a cascade of pathophysiological consequences that encompass all three listed complications:

Heart Failure Development

• Valvular heart disease is a well-established structural cardiac cause of heart failure, with both left-sided and right-sided valve disease leading to progressive ventricular dysfunction 1
• Severe tricuspid regurgitation specifically causes progressive right ventricular dysfunction and increases the risk of heart failure, as sustained severe regurgitation over time leads to significant RV dysfunction 1
• Mitral valve disease with subnormal RV ejection fraction at rest is associated with decreased exercise tolerance and mortality, demonstrating the heart failure consequences of valvular pathology 1
• Flail tricuspid valve is associated with decreased survival and increasing risk of heart failure, indicating that chronic severe valvular regurgitation directly causes heart failure 1

Decreased Ejection Fraction

• Progressive ventricular dysfunction with reduced ejection fraction is a direct consequence of chronic valvular heart disease 1
• In operated patients with mitral valve disease, an RV ejection fraction <20% predicted post-operative death, demonstrating the severity of ejection fraction reduction in valve disease 1
• Aortic stenosis with impaired LV systolic function (ejection fraction <50%) represents a critical stage requiring valve replacement, as myocardial damage progresses through identifiable stages 1
• The prevalence of LVEF <50% in patients at greater than intermediate risk for aortic valve replacement is estimated between 30-50%, highlighting how commonly valve disease causes reduced ejection fraction 1

Sudden Cardiac Death

• Cardiac valvular disease is explicitly listed as a structural cardiac cause of syncope and sudden death in European Heart Journal guidelines 1
• The association of syncope with aortic stenosis has long been recognized as having an average survival without valve replacement of only 2 years, demonstrating the sudden death risk 1
• Structural heart disease, including valvular disease, is a major risk factor for sudden death and overall mortality in patients with cardiac symptoms 1
• Patients with cardiac syncope from structural causes including valve disease had mortality rates of 18-33%, substantially higher than non-cardiac causes 1

Mechanistic Pathways

The progression from valve dysfunction to these complications follows predictable patterns:

• Volume overload from regurgitant lesions leads to ventricular dilation, reduced ejection fraction, and eventual heart failure 1, 2
• Pressure overload from stenotic lesions causes ventricular hypertrophy, myocardial ischemia, and progressive dysfunction leading to heart failure and arrhythmic sudden death 1
• Myocardial damage progresses through four stages in severe aortic stenosis, from no damage (4.4% 1-year mortality) to Stage 4 with significant RV dysfunction (25% 1-year mortality), encompassing all three complications 1

Clinical Significance

• Heart failure with reduced ejection fraction has a 5-year survival rate of only 25% after hospitalization, emphasizing the severity of this complication 3
• The risk of sudden death in heart failure patients, while declining with modern therapies, remains substantial and is directly linked to the presence of structural valve disease 4, 5, 6
• Patients with advanced heart failure and mean ejection fraction of 20% had sudden death risk of 45% at 1 year, demonstrating the interconnection of these complications 1

Critical Clinical Pitfall

The most important pitfall is underestimating the severity of valve disease before irreversible ventricular dysfunction develops 1, 2. Early intervention is crucial to address valvular pathology before ejection fraction decline becomes irreversible and before the risk of sudden death or heart failure becomes prohibitive 1, 2.