Pathologies Altering the Wiggers Diagram During Ventricular Systole
Ventricular systolic phases are altered by conditions affecting contractility, afterload, valve function, and ventricular-arterial coupling, with the most dramatic changes occurring in severe aortic stenosis, heart failure with reduced ejection fraction, and primary valvular regurgitation.
Key Pathophysiologic Alterations During Systole
Isovolumic Contraction Phase Changes
Aortic stenosis causes prolonged isovolumic contraction as the left ventricle must generate higher pressures to overcome the stenotic valve, delaying aortic valve opening and extending this phase 1. The severity of muscle hypertrophy directly correlates with prolonged isovolumic relaxation time 1.
Left ventricular systolic dysfunction demonstrates reduced peak positive dP/dt during isovolumic contraction, reflecting impaired contractility 1, 2. The time-varying elastance (ΔP/ΔV) is reduced, indicating decreased ventricular contractile efficiency 2.
Right ventricular pathology fundamentally differs from left ventricular mechanics—the normal right ventricle lacks distinct isovolumic phases entirely, with ejection continuing into early diastole 3, 4. In right ventricular failure, this characteristic trapezoid-shaped pressure-volume loop becomes further distorted 3.
Ejection Phase Alterations
Severe aortic stenosis produces a characteristic pressure gradient across the valve throughout systole, with peak left ventricular pressure occurring well before end-ejection 1. The ejection fraction may remain normal initially despite severe stenosis when compensatory hypertrophy is adequate 1.
Dilated cardiomyopathy shows reduced end-systolic elastance (Emax), the slope of the end-systolic pressure-volume relationship, which is the gold standard measure of contractility 3, 2. The pressure-volume loop shifts rightward with reduced stroke volume despite increased end-diastolic volume 3.
Mitral regurgitation creates a parallel pathway for left ventricular ejection, reducing forward stroke volume while the total ejection fraction may appear preserved 1. Severe mitral regurgitation causes premature termination of forward flow and diastolic mitral regurgitation when left ventricular end-diastolic pressure is markedly elevated 3.
Aortic regurgitation increases left ventricular end-diastolic volume and stroke volume to maintain forward cardiac output, creating eccentric hypertrophy with chamber dilation 3.
Ventricular-Arterial Coupling Abnormalities
Optimal energetic efficiency requires matching of ventricular elastance to arterial elastance 2. When this coupling is disrupted, the fraction of energy expended without mechanical work increases, and energy is lost during ejection across the aortic valve 2.
Hypertensive heart disease increases left ventricular afterload, causing concentric hypertrophy with increased wall thickness relative to chamber size 3. End-systolic wall stress increases proportionally to intracavitary pressure and chamber diameter, inversely related to wall thickness 3.
Right ventricular afterload sensitivity is extreme—the RV has a shallower end-systolic pressure-volume slope than the LV, resulting in minor increases in afterload causing large decreases in stroke volume 3. Peak RV pressure occurs before end-systolic ejection, creating the characteristic trapezoid RV pressure-volume loop 3.
Specific Valve Pathologies
Tricuspid Regurgitation
Primary tricuspid valve pathology (endocarditis, Ebstein's anomaly, carcinoid syndrome, trauma from pacemaker leads) causes severe regurgitation even with normal pulmonary artery pressures 5. The critical distinction is pulmonary artery systolic pressure remaining <55-60 mmHg despite severe regurgitation 5.
Functional tricuspid regurgitation from right ventricular dilation causes annular dilatation and leaflet tethering without elevated pulmonary pressures 5. Chronic atrial fibrillation progressively dilates the tricuspid annulus, present in 70-88% of patients with severe TR 5.
Multiple Valve Stenosis
Rheumatic involvement of multiple valves (mitral, tricuspid, pulmonic) alters systolic dynamics across all affected chambers 6. Mild stenosis may progress slowly over years to decades, requiring echocardiographic surveillance every 3-5 years 6.
Conduction Abnormalities
First-degree AV block >280 msec causes fusion of E and A velocities when combined with impaired relaxation, faster heart rates, or bundle branch block 3. This reduces the E/A velocity ratio due to higher A-wave velocity when atrial contraction occurs before early diastolic flow decreases to ≤20 cm/sec 3.
Ventricular pacing disrupts normal synchronous contraction and relaxation, with near-simultaneous movement of all ventricular segments replaced by dyssynchronous activation 3. This adversely affects both systolic and diastolic function, altering all diastolic variables used for assessment 3.
Pressure-Volume Loop Distortions
Heart failure with reduced ejection fraction shows rightward and downward shift of the entire pressure-volume loop, with reduced stroke volume, increased end-systolic volume, and decreased end-systolic elastance 3, 2. The pressure-volume area (loop plus ESPVR triangle) increases relative to useful mechanical work, indicating reduced efficiency 2.
Restrictive cardiomyopathy demonstrates elevated pulmonary vascular resistance and absence of ventricular interdependence, distinguishing it from constrictive pericarditis 7. The "dip and plateau" or "square root sign" in ventricular pressure tracings is absent in restriction 7.
Constrictive pericarditis shows diastolic equalization of pressures between right and left heart chambers with characteristic ventricular pressure tracings 7. Thickened pericardium on imaging confirms the diagnosis 7.
Clinical Monitoring Parameters
Left ventricular mass index is the most powerful predictor of isovolumetric relaxation rate (p<0.0001), followed by end-systolic volume index (p=0.0002) and peak negative dP/dt (p=0.0029) 1.
Pulmonary capillary wedge pressure is the single most important predictor of transmitral filling pattern (p<0.0001), followed by left ventricular peak negative dP/dt (p=0.002) 1.
Development of symptoms (dyspnea, fatigue, decreased exercise tolerance) indicates disease progression requiring intervention 6. Increasing right ventricular systolic pressure on serial echocardiograms suggests developing pulmonary hypertension 6.