When approximately 20 to 25% of the left ventricular area is inactivated by an aneurysm, cardiac enlargement via the Starling mechanism is required to maintain adequate stroke volume.
Thirteen patients with left ventricular aneurysm due to coronary heart disease were studied by left heart and coronary sinus catheterization, including cineventriculography and measurement of ventricular mechanics and energetics at rest, and in some subjects, during either isoproterenol infusion or supine leg exercise. Eight patients had an aneurysm estimated to comprise greater than 20% of the left ventricular surface area, associated with increased left ventricular end-diastolic volume and pressure and mean systolic force. Average isometric rate of pressure rise and mean fiber shortening velocity and distance were uniformly decreased. Five patients had an aneurysm, estimated to comprise less than 15% of the left ventricular surface, associated with normal or nearly-normal left ventricular end-diastolic volume and pressure and mean systolic force. Average isometric rate of pressure rise was normal, but fiber shortening velocity and distance were moderately depressed. Stroke output and cardiac output were reduced in both groups. Aneurysms exhibited either paradoxical systolic expansion or apparent lack of motion (akinesis), or both. A theoretical analysis presented indicated that when approximately 20 to 25% of left ventricular area is inactivated by any pathological process, the degree of shortening distance required of the myofiber to maintain stroke volume exceeds physiological limits, and cardiac enlargement (Starling mechanism) must ensue to maintain adequate ejection of blood. The magnitude of the salutary response of isoproterenol coupled with an increase in mechanical efficiency during catecholamine infusion suggested that myocardial catecholamines were depleted with additional aggravation of heart failure in this disease.
Klein et al. (1967) studied this question.