Pablo A. Guzman

Measurement of absolute left ventricular volume from gated blood pool studies

A new method for obtaining absolute left ventricular volume from gated blood pool studies was evaluated in a torso phantom and in 35 patients who also underwent single-plane contrast ventriculography. Gated 400 left anterior oblique and static anterior views were acquired. Left ventricular volume at end-diastole was given by the ratio of the attenuation-corrected end-diastolic count rate from the gated study to the count rate per milliliter from a blood sample. Attenuation correction was made by dividing the end-diastolic count rate by e ud, where u = the linear attenuation coefficient of water and d = the distance from the skin marker to the center of the left ventricle in the anterior view divided by sin 400 to yield the depth of left ventricle in the left anterior oblique view. In the phantom studies, the correlation between radionuclide and true volume was 0.99 (radionuclide = 1.03 true − 3 ml); the standard error of the estimate was 8 ml. In the patient studies, the radionuclide end-diastolic volume was used to calibrate the left ventricular time-activity curve, yielding left ventricular volume throughout the cardiac cycle. The correlation between radionuclide and angiographic enddiastolic volume was 0.95 (radionuclide = 0.97 angiographic + 3 ml); the standard error of the estimate was 36 ml. The correlation between radionuclide and angiographic end-systolic volume was 0.95 (radionuclide − 1.01 angiographic + I ml); the standard error of the estimate was 33 ml. This method permits direct determination of absolute left ventricular volume without assumptions about the shape of the ventricle or the necessity of using regression equations to convert volume “units” to true volume.

Immediate improvement of dysfunctional myocardial segments after coronary revascularization: Detection by intraoperative transesophageal echocardiography

To ascertain the immediate effects of coronary artery bypass grafting on regional myocardial function, intraoperative transesophageal two-dimensional echocardiograms were obtained in 20 patients using a 3.5 MHz phased array transducer at the tip of a flexible gastroscope. Cross-sectional images of the left ventricle were obtained at multiple levels before skin incision and were repeated serially before and immediately after cardiopulmonary bypass. Using a computer-aided contouring system, percent systolic wall thickening was determined for eight anatomic segments in each patient at similar loading conditions (four each at mitral and papillary muscle levels). Of the 152 segments analyzed, systolic wall thickening improved from a prerevascularization mean value (+/- SEM) of 42.7 +/- 2.9% to a postrevascularization mean value of 51.6 +/- 2.6% (p less than 0.001). Thickening improved most in those segments with the worst preoperative function (p less than 0.001). Chest wall echocardiograms obtained 8.4 +/- 2.3 days after operation showed no deterioration or further improvement in segmental motion compared with transesophageal echocardiograms obtained after revascularization. Thus: regional myocardial function frequently improves immediately after bypass grafting, with increases in regional thickening being most marked in those segments demonstrating the most severe preoperative dysfunction, and this improvement appears to be sustained; and in some patients, chronic subclinical ischemic dysfunction is present which can be improved by revascularization.

Augmentation of regional coronary blood flow by intra-aortic balloon counterpulsation in patients with unstable angina.

Intra-aortic balloon counterpulsation is capable of reducing afterload in patients with unstable angina. Whether it is also capable of augmenting coronary blood flow to poststenotic myocardium is controversial. We studied seven patients receiving maximal drug therapy and requiring balloon pumping for unstable angina as balloon volume and assist ratio were altered. All patients had greater than 90% stenosis of the proximal left anterior descending coronary artery. With maximal augmentation (40 cc balloon volume, 1:1 assist ratio) great cardiac vein flow, representing the efflux from the left anterior descending coronary artery bed, rose from a baseline of 52 +/- 20 to 67 +/- 25 ml/min (mean +/- SD, p = .004) and mean aortic diastolic pressure increased from 77 +/- 13 to 99 +/- 33 mm Hg (p = .004). Increased great cardiac vein flow correlated with increased mean aortic diastolic pressure across changes in balloon volumes (off, 20 cc, 30 cc, and 40 cc) and changes in assist ratio (off, 1:4, 1:2, and 1:1) (p = .02). However, the intermediate balloon volumes produced great cardiac vein flows at an intermediate level between full assist and no assist (p less than .05), whereas the intermediate assist ratios did not augment flow. Thus balloon pumping increased flow to a bed fed by collateral vessels or critical stenoses; this increased flow correlated with increased aortic diastolic pressure, indicating probable loss of autoregulatory ability.

Incomplete filling and incoordinate contraction as mechanisms of hypotension during ventricular tachycardia in man.

We sought to determine mechanisms for decrease of cardiac output and for hypotension during ventricular tachycardia (VT) in man. Two-dimensional and M mode echocardiograms and left ventricular pressure from micromanometer-tipped catheters were obtained in 20 patients before, during, and at the end of induced hypotensive VT. Patients were divided into two groups according to left ventricular function in sinus rhythm as assessed by angiographic ejection fraction (EF) before electrophysiologic study. Group 1 (n = 8) had angiographic EF greater than or equal to 50% in normal sinus rhythm, and group 2 (n = 12) had EF less than or equal to 40%. During VT, left ventricular cavity volume (as indexed by short- and long-axis two-dimensional end-diastolic cavity areas) was markedly reduced in group 1, from 19.7 +/- 2 to 8.6 +/- 2 cm2 (p less than .001) and from 32.0 +/- 8 to 22.5 +/- 7 cm2 (p less than .001), respectively, but was only slightly reduced in group 2, from 34.1 +/- 6 to 31.5 +/- 7 cm2 (p = .044) and from 45.0 +/- 8 to 49.4 +/- 7 cm2 (p = NS), respectively. Conversely, left ventricular systolic function during VT (as indexed by fractional reduction in two-dimensional short- and long-axis areas) was markedly depressed in group 2, from 25.6 +/- 6% to 4.2 +/- 4% (p = .005) and from 13.7 +/- 3% to 1.8 +/- 0.8% (p less than .001), respectively, but remained at control levels in group 1. Left ventricular end-diastolic pressures increased in group 1, from 11.8 +/- 2 to 27.7 +/- 8 mm Hg (p = .005) and did not change in group 2 during VT. Pressure-dimension loops from left ventricular pressure and M mode echocardiographically determined cavity dimensions generated from the end of the VT episodes showed that diastolic pressure-dimension relationships returned to control levels with the first prolonged diastolic interval in group 1 patients, indicating that incomplete relaxation was the mechanism responsible for reduction of cardiac output during VT in these patients. Coordination of contraction and relaxation (indicated by the percent ratio of the pressure-dimension loop area to the area of the rectangle just enclosing the loop) decreased from 37 +/- 11% to 16 +/- 13% in group 2 patients during VT (p = .013) but remained at control levels in group 1 patients. Thus, during VT patients with impaired left ventricular function in sinus rhythm (group 2) developed severe discoordination, and patients with normal or near-normal function (group 1) developed incomplete relaxation to account for stroke volume deterioration and hypotension.

Transseptal pressure gradient with leftward septal displacement during the Mueller manoeuvre in man.

Septal displacement is postulated as an important mediator of ventricular interdependence. During acute right ventricular loading with the Mueller manoeuvre the septum flattens and shifts leftward. To investigate the mechanism of this septal deformation, we measured transseptal pressures in nine patients during Mueller manoeuvres with simultaneous right and left ventricular micromanometers, and left ventricular configuration with two-dimensional echocardiograms. Data were analysed throughout diastole and at end-systole during control and maximum Mueller manoeuvre (-40 to -80 mmHg airway pressure). Leftward septal displacement during the Mueller manoeuvre was evidenced by an increase in septal radius of curvature at end-diastole persisting through end-systole. The left ventricular free wall radius of curvature was unchanged. During the Mueller manoeuvre, the left ventricular cavity area decreased significantly in the cross-sectional view. All Mueller manoeuvres were associated with a decrease in left-to-right ventricular transseptal pressure gradient throughout diastole. There was no significant change in the gradient at end-systole; septal flattening persisted, however, despite a pronounced left to right pressure gradient. Thus, diastolic septal flattening during right ventricular loading is associated with a decreased transseptal pressure gradient but does not require right ventricular diastolic pressure to exceed left ventricular diastolic pressure. The persistence of flattening in systole suggests that once septal shift occurs during diastole, other forces during systole maintain the deformity despite a large intracavitary transseptal gradient.

Effect of nitroprusside on hydraulic vascular loads on the right and left ventricle of patients with heart failure.

We studied the effect of nitroprusside on the hydraulic vascular load of the right and left ventricle in seven patients with severe left ventricular failure. At doses of 0.25–0.75,μg/kg/min, stroke volume increased progressively from 40.1 to 48.6 ml and left ventricular end-diastolic pressure decreased from 24.5 to 11.2 mm Hg. Accompanying this improvement in left ventricular performance were doserelated decreases in mean ventricular pressures, pulmonic and systemic resistances and the lower-frequency components of input impedance moduli. Characteristic impedance and both total and oscillatory external power were decreased in the pulmonic, but not the aortic, vasculature. In this class of patients, right ventricular unloading is a striking and direct effect of nitroprusside and may account, in part, for imnproved left ventricular performance through ventricular interdependence.

Septal geometry in the unloaded living human heart.

Right ventricular loading leads to diastolic septal flattening in man without necessarily requiring right ventricular pressure to exceed left ventricular pressure. This observation suggested that the unstressed septal configuration is flat and that its normal concave shape is due to the left-to-right transseptal pressure gradient. To examine this hypothesis, we studied septal configuration by two-dimensional echocardiography in nine patients with normal global and regional left ventricular function during surgery for coronary artery disease. The transseptal pressure gradient was obtained from pulmonary capillary wedge pressure minus right atrial pressure. Measurements were obtained at control (open chest, intact pericardium [C]), with the pericardium open (OP), on cardiopulmonary bypass (CPB), and after cardiac arrest (CA). There were no changes in any measurements between C and OP or between CPB and CA. Left ventricular end-diastolic cavity area decreased from 16.5 +/- 2.1 cm2 at C to 11.1 +/- 4.5 cm2 after CPB, and further decreased to 8.9 +/- 3.5 cm2 after CA (p less than .001), yet the septum flattened, as shown by an increase in its radius of curvature from 1.7 +/- 0.5 cm during C to 2.5 +/- 0.7 cm after CPB, and to 2.9 +/- 1.0 cm after CA (p less than .001), or from 0.4 +/- 0.1 to 0.8 +/- 0.4 to 1.1 +/- 0.5 U (p less than .001) when normalized for cavity area. Diastolic transseptal pressure gradient was reduced from 4.1 +/- 2.3 mm Hg during C to 1.1 +/- 1.8 mm Hg after CPB, and to 0.5 +/- 1.4 mm Hg after CA (p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Regional Coronary Blood Flow During Relief of Pacing-Induced Angina by Nitroglycerin Implications for Mechanism of Action

The mechanism for the therapeutic effect of nitroglycerin in stress-induced angina remains controversial; it has been attributed to both increased blood supply to the ischemic myocardium and decreased myocardial oxygen demand. To investigate the contribution of each of these mechanisms, systemic pressures and great cardiac vein flow were measured in 14 patients with single-vessel disease involving the left anterior descending (LAD) coronary artery during the development of pacing-induced angina and after the administration of nitroglycerin while continuing pacing at the angina-provoking rate. Great cardiac vein flow, measured by thermodilution, represents the venous efflux from the LAD territory and therefore provided an index of flow to the poststenotic myocardium. In 11 patients, nitroglycerin was administered systemically (400 to 800 micrograms sublingually or 200 micrograms intravenously); angina was relieved in 10, concomitant with a decrease in both great cardiac vein flow (from 123 +/- 29 to 98 +/- 29 ml/min, p less than 0.001) and mean aortic pressure (from 118 +/- 22 to 104 +/- 22 mm Hg, p less than 0.001). In contrast, when 75 micrograms of nitroglycerin was administered directly into the left main coronary artery of 7 patients, it produced a small increase in great cardiac vein flow (from 108 +/- 32 to 125 +/- 31 ml/min, p = 0.059), no change in aortic pressure, and no relief of angina. This study suggests that nitroglycerins major beneficial action in pacing-induced angina is unrelated to direct effects on the coronary circulation and is likely related to its cardiac unloading effect.