Biomedical subjects

J E Isea

Publications and source records attributed to J E Isea.

7 recordsLinked to original sources

PubMed1998

Metabolic modulation of acute myocardial infarction. The ECLA (Estudios Cardiológicos Latinoamérica) Collaborative Group.

BACKGROUND: Several trials have been performed in the past using glucose, insulin, and potassium infusion (GIK) for the treatment of acute myocardial infarction (AMI). Because of continuing uncertainty about the potential role of this therapeutic intervention, we conducted a randomized trial to evaluate the impact of a GIK solution during the first hours of AMI. METHODS AND RESULTS: Four hundred seven patients with suspected AMI admitted within 24 hours of symptoms onset were enrolled. In a ratio of 2:1, 268 patients were allocated to receive GIK (high- or low-dose) and 139 to receive control. Phlebitis and serum changes in the plasma concentration of glucose or potassium were observed more often with GIK. A trend toward a nonsignificant reduction in major and minor in-hospital events was observed in patients allocated to GIK. In 252 patients (61.9%) treated with reperfusion strategies, a statistically significant reduction in mortality (relative risk [RR] 0.34; 95% CI: 0.15 to 0.78; 2P=0.008) and a consistent trend toward fewer in-hospital events in the GIK group were observed. CONCLUSIONS: Our results confirm that a metabolic modulation strategy in the first hours of an AMI is feasible, applicable worldwide, and has mild side effects. The statistically significant mortality reduction in patients who underwent a reperfusion strategy might have important implications for the management of AMI patients. It is now essential to perform a large-scale trial to reliably determine the magnitude of benefit.

Cardioplegic Solutions↗

PubMed1994

Load dependence of changes in forearm and peripheral vascular resistance after acute leg exercise in man.

1. It is known that acute exercise is often followed by a reduction in arterial blood pressure. Little is known about the time course of the recovery of the blood pressure or the influence of the intensity of the exercise on this response. Controversy exists, in particular, concerning the changes in peripheral resistance that occur during this period. 2. Eight normal volunteers performed, in random order on separate days, voluntary upright bicycle exercise of three different intensities (maximal, moderate and minimal load) and, on another day, a control period of sitting on a bicycle. They were monitored for 60 min after each test. 3. Diastolic pressure fell after maximal exercise at 5 min (-15.45 mmHg) and 60 min (-9.45 mmHg), compared with the control day. Systolic and mean pressure also fell (non-significantly) after 45 min; heart rate was significantly elevated for the whole hour of recovery (at 60 min, +7.23 beats min-1). No changes in post-exercise blood pressure and heart rate were observed on the days of moderate and minimal exercises. 4. An increase in cardiac index was observed after maximal exercise compared with control (at 60 min, 2.6 +/- 0.3 vs. 1.9 +/- 0.2 l min-1 m-2). This was entirely accounted for by the persistent increase in heart rate, with no significant alteration in stroke volume after exercise on any day.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Time course of haemodynamic changes after maximal exercise.

The haemodynamic changes during 4 h following maximal upright bicycle exercise were evaluated in six normals in a randomized controlled crossover design. Total peripheral resistance was reduced to 2 h (-6.7 mmHg min l-1, P < 0.05); exercising and non-exercising vascular beds were vasodilated for 2 h (-24.1 and -23.8 mmHg min ml-1 100 ml-1 tissue, respectively, P < 0.05), associated with reductions in systolic (-5.8 mmHg, P < 0.05) and diastolic pressure (-8.3 mmHg, P < 0.05). Rise in cardiac index for 1 h (+0.51 min-1 m-2, P < 0.05) was accounted for by an elevated heart rate (+14.4 beats min-1, P < 0.01) as stroke volume was unchanged. Body temperature was elevated until 40 min (+0.20 degrees C, P < 0.05). The return of all haemodynamic variables to control by 3 h suggests a 3 h limit for a hypotensive effect of exercise. Rise in body temperature is not the only factor responsible for the hypotension.

Adult↗

PubMed1992

Ascending aortic Doppler velocity and the prediction of exercise capacity in post-infarction left ventricular dysfunction.

A system to improve analysis of the aortic pulsed Doppler velocity signal has been developed and used to study cardiac performance during a 4 min, 25 W incremental stage supine bicycle exercise to exhaustion. Twenty-two male subjects with stable chronic ischaemic heart disease were studied (15 with NYHA class II/III heart failure, and seven age-matched class I subjects). None had evidence of reversible ischaemia. Peak velocity (PV) from the intensity weighted mean velocity profile, early acceleration (eA) and stroke distance (SD) were all significantly lower at rest in class II/III compared to class I. For the change from rest to 50 W, PV did not alter, eAC increased significantly (P less than 0.05) and to a similar extent in both groups (18.6% class II/III vs 16.4% class I) and SD was reduced from 7.8 to 5.9 in class II/III (P less than 0.01) but did not change in class I (12.4 vs 11.8, ns). There was also a greater increase in heart rate (HR) in class II/III subjects (P less than 0.05). The duration of exercise was correlated with resting PV (r = 0.48, P less than 0.025) but was correlated best with the change in blood momentum (PV x Stroke volume x HR) between rest and peak exercise (r = 0.80, P less than 0.001). Thus Doppler velocimetry can give quantitative information on the response to exercise which discriminates between grades of ventricular dysfunction and is predictive of exercise capacity.

Adult↗

PubMed1991

Cardiac and blood pressure responses to mental stress in reactive hypertensives.

To study the haemodynamic response to a standardized mental stress, we measured ascending aorta velocity using Doppler ultrasonography in 20 reactive ("white-coat") hypertensives and 20 age and sex matched normal controls (NC) familiar with the hospital setting. Reactive hypertensives (RH) had 3 office diastolic BP recordings between 90-110 mmHg and ambulatory BP less than 140/90 mmHg. The cardiac response to mental arithmetic was greater in RH than NC (minute distance, RH: +36.7 +/- 40.2% vs NC: +10.3 +/- 19%, p less than 0.05; peak velocity, RH: +8.4 +/- 16.5% vs NC: -1.4 +/- 11.9%, p less than 0.05), and there was a different peripheral resistance response (RH: -12.2 +/- 24.2% vs NC: +6.5 +/- 22%, p less than 0.05). We suggest that subjects with reactive hypertension have a strong cardiac response to mental stress and this could be a characteristic of this condition.

Adult↗

PubMed1989

Ambulatory pressure monitoring in the assessment of antihypertensive therapy.

A low-cost, ambulatory blood-pressure monitor has been calibrated and validated against a random zero sphygmomanometer. The repeatability of ambulatory pressure recordings after a placebo month in 44 mild to moderate untreated hypertensives was assessed. Systolic blood pressure showed a mean difference over 1 month of 2.0 mmHg, with a standard deviation of differences of 9.3 mmHg. The diastolic blood pressure mean difference was 0.1 mmHg (SD = 6.3 mmHg). This variability was much less than for clinic readings (SD = 17.3 mmHg) or for single home pressure readings (SD = 19.7 mmHg). Using ambulatory monitoring to detect a drop in pressure of 8/5 mmHg with a power of 0.9, the number of subjects needed in a parallel group trial is reduced from 360 to 68, and in a crossover study from 88 to 16 subjects. The usefulness of ambulatory pressure monitoring is demonstrated in a placebo-controlled comparison of atenolol, nifedipine retard, or their combination in random order. Eleven subjects, 21-60 years, with initial average blood pressures of 166.5/104.7 mmHg, showed a reduction in pressure with atenolol 50 mg a day of 15.1/10.0 mmHg, with nifedipine retard 20 mg b.i.d. of 21.0/11.6 mmHg, and with atenolol 50 mg and nifedipine retard 20 mg once a day of 26.2/16.8 mmHg. Ambulatory monitoring of pressure improved the accuracy of the trial and demonstrated a reduction in the alerting response with atenolol.

Adult↗

PubMed1989

Systemic and forearm vascular resistance changes after upright bicycle exercise in man.

1. Blood pressure, cardiac function and forearm blood flow following voluntary maximal upright bicycle exercise were studied in thirteen normal volunteers in a cross-over design against a control day. 2. After exercise there was a short-lived (5-10 min) increase in systolic blood pressure, peak aortic blood velocity and aortic acceleration suggesting a persistence of the positive inotropic influence of exercise. 3. Systemic vasodilation, which was seen immediately exercise stopped, lasted at least 60 min. This was associated with a reduction in diastolic blood pressure for the whole hour. After 30 min systolic blood pressure was also reduced. Heart rate and cardiac output were still significantly elevated and systemic vascular resistance still reduced at 60 min post-exercise. 4. A non-exercising limb vascular bed (forearm) showed a marked vasodilation for 1 h after predominately leg exercise indicating the presence of a vasodilatory influence affecting vascular beds other than the exercising muscle groups.

Adolescent↗