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The catheterization laboratory continues to evolve with time, initially concentrating on hemodynamic assessment of the heart and, in particular, valvular heart disease, before becoming very “coronary-centric” with the advent of balloon angioplasty and the heightened prevalence of coronary artery disease. As we enter the next phase of evolution, the catheter-based treatments of structural heart disease are bringing back some of the early lessons of the importance of ventricular performance and its evaluation. Complicating the transition is the need to synthesize information across multiple noninvasive and invasive modalities of cardiac assessment to determine clinical decision making for individual patients.

Left ventricular dysfunction may occur in the setting of impairment of systolic performance, diastolic performance, and/or abnormal hemodynamic loading conditions. Although, an in-depth understanding of left ventricular mechanics does not directly translate into improved day-to-day clinical practice for the interventional cardiologist, a general understanding of the factors impacting left ventricular performance remains imperative to appropriate therapeutic decisions.


In the cardiac catheterization lab, ventricular pathophysiology is most frequently recognized by the performance of left ventricular (LV) wall motion seen on the left ventriculogram. The left ventriculogram visually portrays the relationship between stroke volume and the end-diastolic volume, and either quantitatively or qualitatively, an ejection fraction is determined. Universally, ejection fraction has been accepted as an estimate of the global LV contractile state. Furthermore, an assessment of regional LV function by wall motion on ventriculography has become an essential part of every cardiac catheterization.1

Qualitative assessment of LV function rests on the visual appreciation between stroke volume and end-diastolic volume. An increase in end-diastolic volume (ie, dilated LV chamber size) is commonly seen in patients with volume overload states (eg, aortic insufficiency). However, stroke volume (ie, the difference between end-diastolic and end-systolic volumes, also known as ejection fraction) is dependent on the myocardial contractile state and, in part, loading conditions. A reduction in the ventricular contractile state may be secondary to intrinsic myocardial disease (ie, nonischemic cardiomyopathy) or may be secondary to coronary artery disease and its associated regional wall motion abnormalities.

Depressed regional wall motion, defined as hypokinesis, reflects a decrease in the contractile state of a particular region of the left ventricle. Noncontraction of a region (akinesis) or outward contraction of a segment during systole (dyskinesis) may reflect the occurrence of a prior myocardial infarction.2 Commonly, the left ventricle is imaged in a right anterior oblique projection, giving good assessment of the anterior-basilar, anterolateral, apical, diaphragmatic, and posterior-basilar segments (Fig. 10-1). In select cases involving the lateral LV wall, the left anterior oblique projection is used to estimate the lateral, posterior, and septal walls. Assessment of regional wall motion is critical to risk stratification and management of patients with coronary artery disease.


An end-diastolic frame taken from a ...

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