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.

Several methods are available to quantify the measurement of ejection fraction from the angiographic image by online software. One method is the so-called area-length method. This method assumes an ellipsoid shape to the ventricle. Calculations of ventricular volume are made from the end-systolic frames and end-diastolic frame using the dimensional measurements of the ventricle. Regression equations correct for the overestimation of the calculated volume to the true volume.^3,4 A second method, the center line method,⁵ has also been used because of its ability to quantify both regional wall motion as well as ejection fraction. This method does not assume a geometric configuration of the ventricle and measures the shortening fractions of 100 chords, which are constructed perpendicular to a centerline that is drawn midway between the end-diastolic and end-systolic contours.

Despite the wealth of information obtained during the performance of ventriculography, practice patterns are highly variable with respect to its current performance. In a recent evaluation of practices across Veterans Affairs (VA) catheterization labs over the years 2000 to 2010,⁶ more than 450,000 catheterizations were performed, and only 58% of those procedures involved left ventriculography. In fact, when looking at the trend of performance over that decade, there was a significant drop over time (Fig. 10-2). Furthermore, there was marked variation among VA facilities in the frequency of performance of ventriculography that could not be explained by patient or clinical factors. Thus, the operator preferences seemed to predominate regarding obtaining ventriculography.

In current practice, there are multiple options available to the operator in assessing LV function, and often, patients present to the catheterization lab with prior noninvasive testing. In an evaluation of a health maintenance organization population, more than 90,000 catheterization procedures performed over the course of a year were administratively evaluated.⁷ Almost 82% of these patients had concomitant performance of left ventriculography, despite the fact that 41% of these same patients had already had noninvasive assessment within the preceding 30 days. Although this does not in itself allow conclusions to be drawn on an individual case-by-case basis, operators must be versed in the value of the noninvasive imaging testing performed prior to catheterization.

Transthoracic echocardiography has become a standard tool for the assessment of LV function. As with cardiac ventriculography, echocardiography allows the assessment of global LV function as well as regional wall motion in the 3-dimensional chamber. Furthermore, it has the ability to better assess coexistent valvular disease (whereas ventriculography essentially only evaluates for mitral regurgitation), especially for aortic and mitral pathology. In addition, assessment of the tricuspid regurgitation jet permits an estimate of right ventricular pressure and systolic function, which can alert the clinician to impaired hemodynamics that may require further evaluation. Furthermore, analysis of mitral inflow patterns and tissue Doppler signals gives great insight into ventricular mechanics, including diastolic dysfunction and restrictive physiology. Radionuclide ventricular imaging also possesses the ability to measure LV volume, ejection fraction, and regional wall motion by the adaptation of gated image acquisition techniques. By the same token, recent advances in contrast computed tomography and magnetic resonance imaging technologies have provided these noninvasive imaging techniques with the ability to evaluate LV size and function.

A large number of clinical trials have been performed to show the reliability of ejection fraction assessed by both radionuclide imaging and echocardiography. In a clinical practice, single-center cohort of unselected patients, there was a close correlation between measurements by these modalities and invasive ventriculography.⁸ There tended to be an overestimate of ejection fraction by echocardiography in the lower range of the measurements compared with ventriculography. Furthermore, nuclear imaging tended to overestimate ejection fraction compared with ventriculography at the lowest values and underestimate it at the higher values. Although all 3 modalities have some variability and are not interchangeable in a 1-to-1 fashion, the absolute variability between measurements was not found to affect clinical decision making.

Pressure-Volume Relationships

A great deal of work has been done in evaluating the interdependence of the multiple factors affecting overall LV performance. The earliest means to understanding LV pump function was the assessment of the LV pressure-volume loop (Fig. 10-3).^9,10 The lower portion of this loop (from left to right in Fig. 10-3) illustrates ventricular filling from the opening of the mitral valve (D) to end diastole (A). A steep increase in pressure occurs from end diastole to the opening of the aortic valve (B), and this is represented on the right side of the loop. The top of the loop begins at aortic valve opening (right to left) and ends at aortic valve closing (C), representing the stroke volume. The left side of the loop represents isovolemic relaxation between the closure of the aortic valve and the opening of the mitral valve.