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R L Engler

Publications and source records attributed to R L Engler.

65 records · Page 4Linked to original sources

Relative effects of nitroglycerin and nitroprusside during experimental acute myocardial ischemia.

When given during acute myocardial infarction (AMI), vasodilators such as nitroglycerin (TNG) and nitroprusside (NP) improve some of the hemodynamic determinants of myocardial oxygen demand. TNG has been shown to reduce ischemic injury during AMI, but variable results have been noted with NP therapy. To compare the effects of these two agents, 8 closed chest sedated dogs with pre-existing multi-vessel coronary constrictions underwent repeated, random-order, acute 15-min balloon occlusions of the left anterior descending coronary artery during the following conditions: (1) saline infusion (control), (2) TNG infusion, and (3) NP infusion. The severity of myocardial ischemia was estimated by summating the ST-segment elevations (xi ST) measured from 7 intramyocardial electrodes; mean left atrial pressure (LAP), heart rate (HR), and mean systemic arterial pressure (SAP) were also measured. No dog had left ventricular failure either before or after occlusion. Since HR and SAP responses to TNG and NP are different, the dogs were randomized into two subgroups: TNG and NP were infused in 4 dogs to produce similar increases in HR (10--20% greater than control), and in the other 4 to produce similar decreases in SAP (15--20% less than control). In each subgroup, xi ST was significantly lower following TNG than following NP. Moreover, in the total group of 8 dogs, xi ST after 10 min of occlusion averaged 38 +/- 10 mV during TNG treatment compared to 46 +/- 10 mV during control occlusion (P less than 0.05). In contrast, xi ST after 10 min of occlusion averaged 57 +/- 11 mV during NP treatment (P less than 0.01 compared to control occlusion). Thus, (1) when given to achieve similar hemodynamic changes following acute coronary occlusion, TNG reduced while NP increased myocardial ischemia, (2) although both 'vasodilators', TNG and NP appear to have different actions on various vascular beds, and (3) the hemodynamic changes induced by vasodilators do not in themselves provide an accurate index of directional alterations in myocardial ischemia.

Animals↗

Effects of equiblocking doses of nadolol and propranolol on left ventricular performance.

Nadolol, a recently developed noncardioselective beta-adrenergic blocker, has the potential advantages of a longer oral half-life (t 1/2) than propranolol and, in animal studies, markedly fewer direct myocardial depressant effects. Neither the relative intravenous potency of nadolol and propranolol nor the comparative effects of the 2 drugs on left ventricular performance has been studied in man. We compared equiblocking intravenous doses of nadolol and propranolol in 10 subjects with ischemic wall-motion disorders. Nadolol was on the average 6.2 times as potent on a milligram-for-milligram basis. Both drugs decreased resting heart rate (p less than 0.02) and produced small rises in both mean pulmonary artery (p less than 0.03) and mean pulmonary artery wedge (p less than 0.03) pressures without significantly reducing the cardiac output. Both drugs also produced depression of the radionuclide ejection fraction (p less than 0.002). There were no significant differences between the effects of the 2 drugs on any of the aforementioned variables. Thus, the effects of nadolol on left ventricular performances are similar to those of propranolol. Because of its long oral t 1/2, nadolol may prove to be a clinically useful drug.

Adrenergic beta-Antagonists↗

Measurement of left ventricular ejection fraction by mechanical cross-sectional echocardiography.

Cross-sectional echocardiography is a new noninvasive technique for imaging the heart. We developed a method for using mechanical cross-sectional echocardiograms (sector scans) to determine left ventricular volumes and ejection fraction. Using left ventricular cineangiography as a standard, sector scan ejection fraction correlated better (r = 0.93) than M-mode echocardiography by any of three established methods, and the sector scan regression line did not differ from the line of identity (p greater than 0.33). Interobserver variability for sector scan ejection fraction was 2.3 +/- 1.2% (mean +/- SD). Variation between two studies performed within 24 hours and analyzed by the same observer was 1.4 +/- 1.5%. However, the sector scans consistently underestimated left ventricular end-diastolic volume. We conclude that sector scan echocardiography is more reliable than conventional M-mode technique for estimating left ventricular ejection fraction, but estimation of left ventricular end-diastolic volume is unreliable with the methods currently available.

Blood Volume↗

The electrocardiogram in asymmetric septal hypertropy.

Electrocardiograms and echocardiograms in 44 patients with asymmetric septal hypertrophy were reviewed. Patients with asymmetric septal hypertrophy had incidences of left ventricular hypertrophy (33 percent; 16/44) and left atrial hypertrophy (25 percent; 11/44) by ECG that were less than in a group of patients with significant aortic stenosis (70 percent [31/44] and 64 percent [28/44], respectively). Left ventricular hypertrophy on the ECG was associated with a greater septal-posterior wall thickness ratio in asymmetric septal hypertrophy. A small Q wave in lead V4 or a ratio of the R-wave to the S-wave amplitude (R/S ratio) of greater than 0.20 in lead V1 was found in 14 of 44 patients with asymmetric septal hypertrophy but in no patients with aortic stenosis. The mean corrected Q-T interval (Q-Tc) of patients with asymmetric septal hypertrophy was prolonged, and the mean Q-Tc of patients with aortic stenosis was normal. The distinctive findings of an R/S ratio of more than 0.2 in lead V1 and Q waves in lead V4 in asymmetric septal hypertrophy have clinical significance, and the prolonged Q-T interval may relate to sudden death.

Adult↗

Hemodynamic compromise associated with ventriculoatrial conduction following transvenous pacemaker placement.

Ventriculoatrial conduction complicating ventricular pacing in a patient with ischemic heart disease led to severe clinical disability and hemodynamic compromise. Data obtained at cardiac catheterization documented that ventriculoatrial conduction of the patients' paced beats led to inadequate left ventricular filling pressures, pulmonary congestion and depressed cardiac output. This complication of ventricular pacing can be suspected at bedside examination and emphasizes the importance of considering the possible hemodynamic effects of ventricular pacing when long-term pacemaker therapy is contemplated.

Aged↗