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Biomedical subjects

H Boudoulas

Publications and source records attributed to H Boudoulas.

At least 163 records · Page 9Linked to original sources
PubMed1979

Malignant premature ventricular beats in ambulatory patients.

The characteristics of premature ventricular beats predisposing to ventricular tachycardia or fibrillation were assessed by 24-h ambulatory monitoring and maximal treadmill exercise testing in 339 cardiac patients with premature ventricular beats. Premature ventricular beats were divided into early (Q-premature ventricular beat less than QT), late (within the last 20% of the cardiac cycle), and midcycle. Ventricular tachycardia was recorded in 45 patients and ventricular fibrillation, in three. The frequency of ventricular tachycardia or fibrillation was 32% in patients with late, 16% in patients with early, and 7% in patients with midcycle premature ventricular beats (P less than 0.05). Patients with frequent (less than 10/min) multiformed premature ventricular beats had a frequency of ventricular tachycardia or fibrillation of 44%, while only 13% of patients with frequent uniformed premature ventricular beats had ventricular tachycardia (P less than 0.05). Ambulatory patients with ventricular tachycardia or fibrillation have frequent multiformed premature ventricular beats, and the ventricular tachycardia or fibrillation is usually triggered by late premature ventricular beats.

Adult↗
PubMed1978

Safety and rationale for continuation of propranolol therapy during coronary bypass operation.

Thirty consecutive patients undergoing coronary bypass were studied. Oral propranolol therapy was maintained up to 4 to 10 hours before operation. Nineteen of the patients had a history of myocardial infarction (MI), 14 had hypoakinetic areas, and 8 had decreased ejection fraction indicating advanced coronary artery disease. Twenty-four-hour urinary epinephrine and norepinephrine obtained the day before operation were markedly increased at 136 +/- 12 microgram per 24 hours (normal, 39 +/- 4 microgram, rho less than 0.01). There were 4 perioperative MIs (13%) and no deaths. Plasma propranolol 1 hour before operation was 43.3 +/- 8 ng per milliliter, indicating good beta blockade. Propranolol was started within 24 hours postoperatively. There were no preoperative, intraoperative, or postoperative complications related to propranolol therapy. We conclude that because of markedly increased adrenergic tone the day before operation and transient hypersensitivity to adrenergic stimulation after withdrawal of propranolol, this agent should be continued through coronary bypass operation.

Adult↗
PubMed1978

Systolic time intervals in atrial fibrillation.

Forty patients with atrial fibrillation and 20 patients with congestive heart failure and sinus rhythm were studied. Patients were divided into two groups. Group A consisted of 20 patients with atrial fibrillation in whom systolic time intervals were measured. Twenty to 50 beats were analyzed. Five of the patients had high-fidelity measurements of left ventricular pressure simultaneous with determination of systolic time intervals. Analysis of the systolic time intervals for the entire group showed that the preejection period lengthened at faster heart rates and that the left ventricular ejection time was relatively constant at slower heart rates. This resulted in a progressive increase in the ratio of preejection period over left ventricular ejection time (PEP/LVET) as the heart rate increased. The rate of increase in PEP/LVET was minimal below a heart rate of 75 beats per minute. The increase in preejection period at faster heart rates is due to greater isovolumic developed pressure without a corresponding increase in left ventricular dp/dt. Group B consisted of 40 additional patients (20 with atrial fibrillation and 20 with sinus rhythm). In group B, the total electromechanical systole corrected for heart rate (QS2I) and the levels of digoxin in the blood were compared. The QS2I was significantly shorter in atrial fibrillation (497 +/- 5 msec vs 528 +/- 4 msec; P less than 0.01), while the levels of digoxin in the blood were identical (0.9 +/- 0.1 vs 1.0 +/- 0.1 ng/ml). The results of this study must be considered when systolic time intervals are to be employed in patients with atrial fibrillation.

Adult↗
PubMed1977

A critical review of the systolic time intervals.

The theoretical basis for the use of the systolic time intervals has been largely established. The method has been validated by direct measures from within the circulatory system. Standards for equipment and technique have been defined. Numerous clinical studies have demonstrated the value of this quantitative noninvasive technique for assessing left ventricular performance. At present there is need for further studies of the clinical usefulness of the systolic time intervals to improve both diagnosis and therapy of various cardiovascular disorders.

Aorta↗
PubMed1977

Negative inotropic effect of lidocaine in patients with coronary arterial disease and normal subjects.

The effect of administration of lidocaine on left ventricular performance was studied using systolic time intervals in nine normal subjects, eight patients with stable angina, and 15 patients with acute myocardial infarction. The greatest response in systolic time intervals occurred at three minutes after intravenous injection of lidocaine (100 mg), with values returning to baseline at 10 to 15 minutes. Administration of lidocaine produced a significant prolongation of the preejection period (PEP) corrected for heart rate in all groups and a prolongation of the ratio of PEP to left ventricular ejection time (PEP/LVET) in patients with angina. The group with acute myocardial infarction exhibited a hyperadrenergic state, as shown by a short baseline QS2I. The QS I was lengthened by administration of lidocaine in all groups, but this was more profound in those with acute myocardial infarction. These changes in systolic time intervals were still present at two hours after injection in six patients with acute myocardial infarction in whom an infusion of lidocaine followed the initial bolus. The effect of administering lidocaine after intravenous injection of propranolol (5 mg) was also studied in six normal subjects. Although propranolol therapy along prolonged the PEP/LVET, a further significant prolongation followed subsequent injection of lidocaine.

Acute Disease↗
PubMed1977

Hypersensitivity to adrenergic stimulation after propranolol withdrawal in normal subjects.

The cardiac response to isoproterenol after propranolol withdrawal was studied in six normal persons. Serial isoproterenol infusions were done before and after oral propranolol administration, 160 mg daily for 2 days. Changes in electromechanical systole corrected for heart rate (QS2I) and pulse pressure were used to assess the inotropic response to isoproterenol, and changes in heart rate were used to assess the chronotropic response. As shown in previous studies, the negative inotropic effect of propranolol lasted only 12 to 15 h, while the negative chronotropic effect lasted 24 to 36 h. After the disappearance of blockade a hypersensitivity to isoproterenol was found 24 to 48 h after propranolol withdrawal in all three measured determinants. The explanation of this phenomenon most likely lies in the nature of adrenergic receptors that become activated during long-term blockade.

Administration, Oral↗
PubMed1976

Usefulness of systolic time intervals in coronary artery disease.

This review summarizes current knowledge concerning the value of systolic time intervals in coronary artery disease. Although the usual pattern of prolongation of the preejection period (PEP) and shortening of the left ventricular ejection time (LVET) characteristic of left ventricular failure is seen in acute myocardial infarction, the systolic time intervals (as well as all other measures) are profoundly influenced by adrenergic hyperactivity characteristics of this disorder. Adrenergic stimulation normally shortens both the PEP and LVET indexes and decreases the PEP/LVET ratio. The degree of shortening of electromechanical systole (QS2) is directed related to the excessive adrenergic tone. Patients with the greatest systolic time interval abnormalities have a poorer prognosis, a greater incidence of congestive heart failure and more abnormalities of directly measured indexes of left ventricular performance. The systolic time intervals are useful for assessing left ventricular performance in chronic coronary artery disease as well. In chronic coronary artery disease the PEP/LVET ratio and angiographically determined left ventricular ejection fraction are closely correlated ( r = -0.76), but the level of this correlation is less than that in other forms of left ventricular disease. The left ventricular ejection time index is prolonged after exercise in patients with angina pectoris when compared with findings in normal subjects. Failure of the ischemic ventricle to respond to adrenergic stimulation is the most likely mechanism. Addition of the postexercise left ventricular ejection time to standard treadmill stress testing identifies a significant number of patients (23 percent) who would have had false negative results by electrocardiographic criteria alone. In addition, this index provides confirmatory evidence in those with apparently positive electrocardiographic test data. The systolic time intervals have been useful in assessing both medical and surgical therapy in coronary artery disease. The test can be performed repeatedly and provides a measure of both left ventricular performance and extent of adrenergic hyperactivity. Thus, evaluation of therapy represents the most useful future application of systolic time intervals.

Acute Disease↗
PubMed1976

Left ventricular function and adrenergic hyperactivity before and after saphenous vein bypass.

Forty patients with severe angina pectoris were studied before and two weeks after saphenous vein bypass surgery (SVG) in order to assess the effect of this operation on left ventricular performance as judged by systolic time intervals (STI). The patients were divided into two groups: group I included 29 patients in whom no postoperative infarction occurred and group II was composed of 11 patients with postoperative infarction. For group I the PEP/LVET was 0.39 +/- 0.01 preop and slightly but significantly increased at 0.42 +/- 0.004 (P less than 0.025) two weeks postop. The mean preop PEP/LVET was 0.33 +/- 0.01 for group II and dramatically increased to 0.54 +/- 0.02 (P less than 0.001) after surgery. Another striking abnormally was a marked shortening of electromechanical systole (QS2I), which was uniformly present in the postoperative studies. Follow-up studies in 16 patients and urinary catecholamine determination in five patients suggested excessive adrenergic activity was responsible for the abbreviated QS2I. This phenomenon must be considered when interpreting the results of SVG on left ventricular function.

Adult↗
PubMed1975

Left ventricular pressure responses in post-angiographic angina.

Alterations in left ventricular end-diastolic pressure and in dp/dt observed in ten patients with coronary heart disease who developed angina pectoris following left ventricular cineangiography were compared with those of six other patients who developed angina spontaneously and with patients who underwent left ventricular cineangiography without experiencing angina. In the patients with post-angiographic angina there was a greater increase in end-diastolic pressure than that seen in the other patients, but there was no significant change in dp/dt. Changes in left ventricular pressure associated with post-angiographic angina would appear to reflect the combined effects of increased preload provided by the contrast material and of ventricular dysfunction including diminished compliance associated with angina. A rise in end-diastolic pressure greater than 20 mmHg following left ventricular cineangiography should alert the physician that the patient may be having myocardial ischemia.

Angina Pectoris↗
PubMedDate not supplied

Concentration-dependent clearance of procainamide in normal subjects.

Four normal volunteers each received two intravenous doses of PA. The mean low dose was 3.30 mg kg-1 (infused over 20 minutes) while the mean high dose was 12.5 mg kg-1 (infused over 60 minutes). Blood samples were collected for 12 hours and urine was collected for 48 hours after each dose. PA concentrations were determined by both HPLC and fluorescent immunoassay methods. The reported concentrations and pharmacokinetic parameters are from the HPLC data unless otherwise indicated. The mean peak serum PA concentrations resulting from the low and high doses were 3.18 and 9.07 micrograms ml-1, respectively. Total PA clearance averaged 763 ml min-1 and 577 ml min-1 while renal clearance averaged 360 ml min-1 and 318 ml min-1 after the low and high doses, respectively. Concentration-dependent decreases in nonrenal PA clearance ranged from 31 to 43 percent (p less than 0.05) in the four subjects. Total clearance decreases ranged from 4.7 to 36 per cent (p less than 0.05). Differences between doses in renal clearance, elimination rate constant, and volume of distribution were not statistically significant. This study demonstrates that the nonrenal and total clearances of PA are concentration-dependent in normal subjects at therapeutic plasma PA concentrations and suggests that the total clearance changes are of sufficient magnitude to be clinically important.

Acecainide↗
PubMedDate not supplied

Effect of cimetidine on quinidine bioavailability.

Elevations in quinidine steady-state serum concentrations have been reported in patients who received cimetidine concurrently. Studies in normal volunteers have shown that areas under the serum concentration-time curve of orally administered quinidine are higher when quinidine is given during chronic cimetidine therapy as compared to under control conditions. The mechanism for this interaction is generally ascribed to decreased hepatic clearance as a consequence of enzyme inhibition. In this study, we show that cimetidine also decreases the bioavailable fraction of quinidine.

Administration, Oral↗