What are the causes of ventricular hypokinesis?

Causes of Ventricular Hypokinesis

Ventricular hypokinesis results from diverse etiologies, with coronary artery disease, hypertension, and idiopathic dilated cardiomyopathy being the most common causes in the United States, though ischemic heart disease has emerged as the predominant etiology. 1

Primary Cardiac Causes

Coronary Artery Disease and Ischemia

• Coronary artery disease represents the leading cause of left ventricular systolic dysfunction in adults, having surpassed hypertension as detection and treatment programs have improved 1
• Myocardial infarction produces regional hypokinesis corresponding to the affected coronary territory 1
• Hibernating myocardium—chronically hypoperfused but viable tissue—manifests as hypokinetic segments that can improve after revascularization, even with ejection fractions as low as 15-20% 1
• Myocardial stunning from intermittent ischemia causes reversible ventricular dysfunction 1

Cardiomyopathies

• Dilated cardiomyopathy produces global hypokinesis with ventricular dilatation, reduced ejection fraction, and both systolic and diastolic dysfunction 1, 2
• Hypertrophic cardiomyopathy can paradoxically progress to left ventricular hypokinesia, particularly in patients with midventricular obstruction (80% incidence versus 7% in those without) 3
• Stress-induced (Takotsubo) cardiomyopathy causes characteristic apical ballooning with mid-apical hypokinesis, akinesis, or dyskinesis extending beyond single coronary territories 1, 2
• Arrhythmogenic cardiomyopathy produces regional right ventricular hypokinesis and dyskinesis, particularly affecting the right ventricular outflow tract 1

Hypertension

• Long-standing hypertension remains a major secondary cause of dilated cardiomyopathy and global hypokinesis 1

Infectious and Inflammatory Causes

• Viral, bacterial, and fungal myocarditis can produce both regional and global hypokinesis 1
• Acute rheumatic fever affects ventricular function 1
• Cardiac sarcoidosis produces segmental hypokinesis with characteristic findings including mediastinal lymphadenopathy, LV septal scar, and intense PET-FDG uptake 1
• Systemic sclerosis and other collagen vascular disorders (lupus, rheumatoid arthritis, polyarteritis nodosa) cause ventricular dysfunction 1

Toxic and Metabolic Causes

Cardiotoxic Substances

• Chemotherapeutic agents, particularly anthracyclines (doxorubicin) and cyclophosphamide 1, 2
• Alcohol, cocaine, heroin, and amphetamines 1
• Heavy metals: lead, arsenic, cobalt 1
• Other toxins: phosphorus, ethylene glycol, sulfonamides 1

Nutritional and Electrolyte Disorders

• Protein, thiamine, and selenium deficiencies 1
• Hypocalcemia, hypophosphatemia, hyponatremia, and hypokalemia 1

Endocrine Disorders

• Diabetes mellitus, hypothyroidism, hyperthyroidism 1
• Hypoparathyroidism with hypocalcemia, pheochromocytoma, acromegaly 1

Infiltrative Disorders

• Amyloidosis produces characteristic basal-predominant hypokinesis with preserved apical function ("apical sparing" pattern) despite normal ejection fraction 1
• Hemochromatosis and sarcoidosis cause restrictive patterns with associated hypokinesis 1

Arrhythmia-Related Causes

• Tachycardia-induced cardiomyopathy from incessant supraventricular tachyarrhythmias or atrial fibrillation with rapid ventricular rates produces reversible global hypokinesis 1
• Ventricular pacing, particularly at the left ventricular apex, can cause localized hypokinesis due to early shortening and systolic rebound stretch 4

Acute Hemodynamic Causes

Pulmonary Embolism

• Acute massive pulmonary embolism causes right ventricular hypokinesis with characteristic sparing of the RV apex (McConnell sign), though this finding is not entirely specific 1, 5
• Right ventricular dilatation (RV/LV ratio >0.6 or area ratio >1.0) indicates massive embolism 1
• Acute RV pressure overload cannot generate systolic pressures exceeding 60 mmHg; higher values suggest chronic disease 1

Septic Shock

• Global left ventricular hypokinesis occurs in 60% of septic shock patients, with 39% presenting at admission (primary) and 21% developing after 24-48 hours of norepinephrine support (secondary) 6
• This dysfunction is typically reversible with inotropic support and does not confer worse prognosis 6

Valvular Heart Disease

• Chronic aortic stenosis and mitral regurgitation produce progressive ventricular dysfunction through pressure and volume overload 1
• Annular dilatation with secondary valvular regurgitation occurs as a consequence of ventricular remodeling 1

Miscellaneous Causes

• Peripartum cardiomyopathy develops in late pregnancy or early postpartum period 1
• Hypereosinophilic syndrome, Whipple's disease, L-carnitine deficiency 1
• Sleep apnea syndrome contributes to ventricular dysfunction 1
• Anaphylaxis can rarely cause midventricular hypokinesis through mast cell-mediated coronary spasm 7
• Chagas disease remains an important cause in endemic regions 1

Critical Diagnostic Considerations

The designation "idiopathic dilated cardiomyopathy" should only be applied after excluding all specific etiologies through appropriate evaluation 1. When regional wall motion abnormalities are present, careful comparison of coronary angiography and ventriculography is mandatory to identify perfusion-contraction mismatch, as approximately one-third of patients with obstructive coronary disease may have coexisting Takotsubo syndrome 1. Wall motion abnormalities extending beyond single coronary territories suggest non-ischemic etiologies 1.