Julio F. Tubau

Increased plasma catecholamine levels in patients with symptomatic mitral valve prolapse

Total plasma catecholamine levels, plasma norepinephrine levels, heart rate, and systolic and diastolic pressures were measured in 15 symptomatic patients with mitral valve prolapse and in 19 normal subjects in supine baseline conditions and in a standing position. In the 15 symptomatic patients, total plasma catecholamine levels and plasma norepinephrine levels were significantly elevated in both positions, and heart rate was lower than in normal subjects in the supine position but returned to normal in the upright position. Thus, symptomatic patients with mitral valve prolapse demonstrate increased resting sympathetic tone. In addition, the associated supine bradycardia suggested that increased vagal tone might also be present at rest. These observations support the hypothesis of a dual autonomic dysfunction in these patients and could account for some of the clinical manifestations of the mitral valve prolapse syndrome.

QT interval prolongation and increased plasma catecholamine levels in patients with mitral valve prolapse.

The heart rate corrected QT interval (QTc) and plasma catecholamine (CA) and norepinephrine (NE) levels were measured in 15 symptomatic patients with idiopathic mitral valve prolapse (MVP) and in 19 control subjects. MVP patients showed longer mean QTc and were divided into two groups: group A normal QTc (greater than 440 msec) and group B prolonged QTc (less than 440 msec). In supine resting conditions CA levels were as follows: group A 0.420 +/- 0.035 ng/ml and group B 0.619 +/- 0.104 ng/ml (p less than 0.05); both were greater than control values (0.348 +/- 0.017 ng/ml, p less than 0.005). NE levels were as follows: group A 0.350 +/- 0.031 ng/ml and group B 0.376 +/- 0.052 ng/ml (NS); both were greater than control values (0.242 +/- 0.025 ng/ml, (p less than 0.05). When a standing position was assumed, CA and NE levels increased significantly in all groups but this was most marked in group B as compared to control levels (CA: 1.039 +/- 0.123 ng/ml versus 0.625 +/- 0.037 ng/ml; NE: 0.737 +/- 0.076 ng/ml versus 0.504 +/- 0.031 ng/ml) (p less than 0.001 and p less than 0.05, respectively). Thus the longest QTc was observed in patients with MVP who had the highest levels of CA and NE, in both supine and standing positions. These data may account, in part, for the occurrence of severe ventricular arrhythmias in some patients with MVP and may offer a rationale for adrenergic blockade in that subset of patients with MVP and markedly prolonged QTc.

Measurement of left ventricular contractility using transesophageal echocardiography in patients undergoing coronary artery bypass grafting

Optimal assessment of left ventricular function requires the use of load-independent indices of myocardial contractility, which often are difficult to obtain in patients undergoing coronary artery bypass graft (CABG) surgery. We have investigated whether the relation between left ventricular end-systolic stress (ESS) (derived from high-fidelity intraventricular pressure measurements and transesophageal-derived wall thickness) and end-systolic area (ESA) (derived from transesophageal echocardiography [TEE]) could provide a load-independent index of left ventricular function. We studied seven men undergoing coronary revascularization. Multiple data points at varied loading conditions were generated for each patient by infusions of sodium nitroprusside and phenylephrine during the period immediately after induction of general anesthesia and preceding surgical incision. While peak systolic blood pressure was pharmacologically altered between 78 and 204 mm Hg, the correlations between ESS and ESA were excellent for all patients (range r = 0.90 to 0.99). Additionally, the slopes of these relations showed a close correlation to their respective baseline thermodilution cardiac indices (r = 0.85, p = 0.02). Appropriate shifts of the ESS/ESA relationships were documented during postextrasystolic potentiation. The authors conclude that the left ventricular ESS/ESA correlation, derived using TEE and intraventricular pressure measurements, may provide a load-independent index of left ventricular inotropic state in patients undergoing CABG surgery.

Pulmonary blood volume: Relationship to changes in left ventricular end-diastolic pressure during atrial pacing

Little data exist about the relationship between changes in cardiac end-diastolic pressure and changes in pulmonary blood volume. To assess this relationship, we studied 11 patients with coronary heart disease during atrial pacing in an attempt to produce multiple pressure-volume points. During catheterization, we obtained Millar pressure recordings of end-diastolic pressure along with equilibrium radionuclide angiograms. Cardiac output, ejection fraction, and pulmonary blood volume were obtained by means of recently validated radionuclide techniques. During pacing, substantial changes in pulmonary blood volume occurred only with marked increase in end-diastolic pressure volume (greater than or equal to 15 mm Hg) and rarely exceeded 15% of control pulmonary blood volume. Cardiac output did not change, while ejection fraction declined during pacing. There was a fair correlation between the absolute change in pulmonary activity (or pulmonary blood volume) or the percentage of change in pulmonary activity over the control value with end-diastolic pressure when all the data points were evaluated (n = 74, r greater than 0.70). However, the scatter in the data precluded making accurate estimates of pressure changes from changes in radionuclide volume changes. We conclude that large changes in cardiac filling pressure must occur during atrial pacing, where cardiac output does not change, before visible pulmonary blood volume changes occur. This may limit the extrapolation of presumed pressure changes from known pulmonary blood volume when changes are small.

Pulmonary blood volume: correlation of equilibrium radionuclide and dye-dilution estimates.

In fifteen prospective patients with aortic stenosis undergoing transseptal cardiac catheterization, dye-dilution and count-based estimates of pulmonary blood volume (PBV) were performed. Three radionuclide methods were evaluated. Two were based on electrocardiogram (ECG)-gated imaging of the thorax, where pulmonary counts (PC) were corrected for frame-time, venous radioactivity, and either (1) the number of processed heart beats or (2) the total duration of acquisition. The third method involved ungated frame mode acquisitions, where PC were corrected for the duration of acquisition and the venous activity. PC (per channel element) were derived from manual assignments of the right lung. All methods correlated well with standard dye-dilution techniques (r greater than 0.82), though at greater volumes it was clear that count-based methods underestimated the dye-dilution values. In five acutely instrumented, anesthetized dogs, radionuclide (ungated formula) and dye-dilution estimates of PBV were made during multiple interventions (19 data points). The five control count volumes as well as the 14 separate intervention points correlated well (r greater than 0.89). It is concluded that PC from equilibrium blood pool images reflect PBV and that induced changes in PC can be utilized as a reflection of changes in PBV.

Influence of therapy on silent ischemia and ventricular arrhythmias in hypertensive patients.

To assess whether therapy with hydrochlorothiazide (HCTZ) or the calcium antagonist nitrendipine influences silent ischemia or arrhythmias, we studied 10 asymptomatic hypertensive male patients with positive Tl-201 scintigraphy in a double-blind, crossover protocol. Blood pressure (BP) and 48-h Holter monitoring were obtained after 2 weeks of placebo and 8 weeks each of HCTZ and nitrendipine therapy. Ischemia was defined as greater than 1 mm ST-segment depression lasting greater than 1 min and was quantified by the number of episodes, duration, and area under the curve (AUC). The mean number of PVCs per hour and the number of episodes of ventricular tachycardia (greater than 3 beats) were also assessed. Diastolic BP was significantly reduced by both HCTZ and nitrendipine (98 +/- 6 vs. 90 +/- 6 vs. 88 +/- 7 mm Hg, respectively, p less than 0.05), but systolic BP was unchanged for either drug. The number of ischemic episodes was reduced by nitrendipine, from 2.4 +/- 3 to 0.8 +/- 2, (p less than 0.05) but not by HCTZ (2.4 +/- 3 to 1.5 +/- 3, p = NS). The duration of ischemia (37 +/- 43 vs. 5 +/- 9 min, p less than 0.05) as well as the AUC (41 +/- 45 vs. 7 +/- 14 mm/min, p less than 0.05) were reduced only by nitrendipine. The number of PVCs rose with HCTZ therapy, from 19 +/- 34 to 69 +/- 88 (p less than 0.05) and was unchanged by nitrendipine (19 +/- 34 vs. 19 +/- 40, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)