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Increased diastolic time: a possible important factor in the benefical effect of propranolol in patients with
Insights
Propranolol significantly increased diastolic time (DT) in patients with coronary artery disease, allowing more time for coronary perfusion. This effect may be as crucial as reducing myocardial oxygen consumption.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Diastolic time (DT) is inversely related to heart rate (HR).
- Propranolol is a beta-blocker used in cardiovascular conditions.
Purpose of the Study:
- To investigate the effect of propranolol on diastolic time (DT) in patients with coronary artery disease (CAD).
Main Methods:
- Studied 150 patients with CAD, divided into three groups: stable angina, acute myocardial infarction, and post-coronary bypass surgery.
- Administered intravenous and oral propranolol, measuring DT and electromechanical systole (QS2).
- Compared DT in patients on propranolol versus those not on the medication after surgery.
Main Results:
- Propranolol significantly increased DT in all patient groups, with changes mainly attributed to decreased HR.
- Intravenous propranolol increased DT in stable angina, acute myocardial infarction, and post-surgery patients.
- Patients on long-term propranolol therapy exhibited greater DT compared to those not on the medication, both pre- and post-surgery.
Conclusions:
- Propranolol significantly increases diastolic time (DT) per beat in patients with coronary artery disease.
- This increase in DT provides more time for coronary perfusion.
- The effect of propranolol on DT may be a significant therapeutic benefit in CAD management, comparable to its effect on myocardial oxygen consumption.
Abstract:
Diastolic time (DT) calculated as the cycle length minus electromechanical systole (QS2) has a nonlinear relationship to heart rate (HR), increasing rapidly as rates fall below 75. The effect of propranolol on DT was studied in 150 patients with coronary artery disease. Patients were divided into three groups. Group I included patients with stable angina pectoris: propranolol (2.5 mg, i.v.) significantly increased DT from 411 +/- 18 to 527 +/- 22 msec (p less than 0.001) in 23 patients of group I; therapy with propranolol (mean daily dose 200 +/- 15 mg) increased DT from 446 +/- 29 to 766 +/- 26 msec (p less than 0.001) in 15 patients with stable angina. Group II was made up of patients with acute myocardial infarction: Propranolol (2.5 mg, i.v.) increased DT from 379 +/- 16 to 458 +/- 24 (p less than 0.001) in 18 of these patients. Group III included patients with recent coronary bypass surgery: propranolol (2.5 mg, i.v.) increased DT from 323 +/- 9 to 468 +/- 24 msec (p less than 0.001) in 14 patients 7 days after surgery. In addition, DT at 15 hr and 2 weeks after surgery was compared in 30 patients maintained on propranolol (mean daily dose, 155 +/- 11 mg preoperative and 68 +/- 9 mg postoperative) and 50 other patients who underwent coronary bypass surgery not on propranolol. DT was greater in propranolol patients (546 +/- 21 vs. 388 +/- 16 msec, p less than 0.001), preoperative and 396 +/- 15 vs. 320 +/- 12 msec, p less than 0.001, postoperative). Changes in DT after propranolol are mainly attributed to decreased HR. Changes in QS2 were much less profound and always less (p less than 0.01) than changes in DT. Thus propranolol significantly increased DT per beat in patients with coronary artery disease, which allowed more time for coronary perfusion; this effect of propranolol could well be as important as the reduction of myocardial oxygen consumption.