Loss of Contractility and Diastolic Heart Failure
Yes, loss of contractility can be associated with diastolic heart failure, though this represents a complex relationship where both systolic and diastolic dysfunction frequently coexist regardless of ejection fraction. 1
The Coexistence of Systolic and Diastolic Dysfunction
In most patients with heart failure, abnormalities of systolic and diastolic dysfunction coexist, regardless of ejection fraction. 1 This is a critical concept that challenges the traditional binary classification of heart failure:
- Even patients with preserved ejection fraction (HFpEF) typically have some degree of systolic dysfunction, and conversely, patients with reduced ejection fraction invariably have diastolic abnormalities 1
- Diastolic dysfunction commonly coexists with systolic dysfunction and may even represent the predominant physiologic disturbance in many patients 2
- The clinical syndrome of heart failure can result from inadequate myocardial contraction (systolic failure), failure of ventricles to fill at low pressure (diastolic failure), or both 2
When Contractility Loss Indicates Diastolic Dysfunction
Loss of contractility can specifically indicate or contribute to diastolic heart failure through several mechanisms:
Inadequate Hypertrophic Response
- When the hypertrophic process is inadequate and relative wall thickness does not increase proportionally to pressure, wall stress increases and high afterload causes decreased ejection fraction 1
- This represents a failure of compensatory mechanisms where loss of contractility reflects underlying diastolic abnormalities 1
Advanced Hypertrophy with Impaired Relaxation
- Advanced myocardial hypertrophy is associated with increased resistance to ventricular diastolic inflow due to both structural alterations (increased wall thickness, altered collagen matrix) and impaired diastolic relaxation of hypertrophied myocardium 3
- Hypertrophic myocytes demonstrate impaired intrinsic contractility AND relaxation, with hypertrophy causing clinically relevant deterioration of ventricular relaxation and compliance 4
Ischemia-Related Mechanisms
- Myocardial ischemia causes a decline in relaxation rate, increased resistance to early diastolic filling, and striking upward shifts in left ventricular diastolic pressure-volume relationships 3
- Hypertrophied hearts exhibit reduced coronary blood flow per gram of muscle and limited coronary vasodilator reserve, even without epicardial coronary disease 1
Clinical Implications for Diagnosis
The presence of some contractility loss in a patient with suspected diastolic heart failure should prompt specific evaluation:
- Diastolic heart failure diagnosis requires: (1) signs/symptoms of heart failure, (2) normal or slightly reduced LVEF (>50%), and (3) increased diastolic filling pressure 5
- Loss of atrial contraction (as with atrial fibrillation) in patients with diastolic dysfunction often leads to serious clinical deterioration, as forceful atrial contraction plays a critical role in ventricular filling without increasing mean left atrial pressure 1
- Depressed contractile state may be responsible for low ejection fraction, though it's often difficult to determine whether low EF is due to depressed contractility or excessive afterload 1
Pathophysiologic Mechanisms Linking Both
The mechanisms connecting contractility loss to diastolic dysfunction include:
- Increased end-diastolic volume from reduced contractility determines increased wall stress, which further reduces systolic performance and worsens diastolic compliance 4
- Altered calcium handling affects both contraction and relaxation, with changes in sarcoplasmic ATPase activity reducing Ca2+ availability during both phases 4
- The compensatory response to reduced contractility (including neurohormonal activation and hypertrophy) carries unfavorable effects that contribute to further deterioration of both systolic and diastolic function 4
Common Pitfall to Avoid
Do not assume that preserved ejection fraction means absence of contractility problems. The vast majority of patients with HF and relatively preserved LVEF have evidence of left ventricular hypertrophy, and many have detectable structural abnormalities including myocardial scar 1. These patients may have subtle contractility abnormalities that contribute significantly to their diastolic dysfunction, particularly in the setting of hypertension, diabetes, or coronary disease 1.