PubMed Health⌕ Search

Biomedical subjects

S Trevethan

Publications and source records attributed to S Trevethan.

14 recordsLinked to original sources
PubMed1991

Giant T waves simulating apical hypertrophic myocardiopathy that disappear with sodium nitroprusside administration. Case report of pheochromocytoma.

Giant inverted T waves (amplitude greater than 1 mV) in precordial leads have been described in various disease processes. However, the pathophysiology of these anomalies has not been studied in depth. This paper analyzes repolarization abnormalities occurring in a case of pheochromocytoma in which giant T waves were unaffected by alpha-adrenergic blockade but were affected by administration of sodium nitroprusside. It is postulated that the probable cause of this aberration is myocardial ischemia of noncoronary origin resulting from an imbalance of supply and demand of oxygen that is relieved by the hemodynamic action of nitroprusside when left ventricular wall stress is reduced.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

[Detection of early occlusion of aortocoronary by-passes. Usefulness of a non-angiographic method].

A total of 83 bypasses were studied. Angiographic results demonstrated occlusion in 3 of 24 bypass of internal mammary artery placed in the anterior descending artery, 2 in the right coronary artery, 1 in the posterolateral of the circumflex and 1 in the first diagonal branch, with a total occlusion average of 8.4% within the first 8 days. We found a good correlation between the coronarographic angiograms and the positivity or negativity of the echo-electrocardiographic tests, during atrial pacing. We believe that this simple method could be done routinely in all the patients after coronary surgery, to decide the need of a new coronary angiogram. Furthermore, this study shows that the occlusion of a single coronary bypass does not produce myocardial infarction, detectable by enzymatic measures or by resting EKG. This method also detects the early post-operatory sinus sick syndrome.

Adult↗
PubMedDate not supplied

[Endocardial pacemaker misplaced in the left ventricle by arterial retrograde route].

This is a presentation of the only case reported in the literature of a misplaced definitive pacemaker reaching left ventricular endocardium through the left subclavian artery by retrograde route. It did not produce important complications in a four years period. Possible implications resulting from this situation are discussed.

Aged↗
PubMedDate not supplied

[Myocardial ischemia in aortic stenosis].

In hypertensive heart disease without coronary artery disease it has been proposed that the presence of ischemia of myocardial tissue is due to an inadequate increment of myocardial mass or to an increase in coronary artery resistance. In this study, 18 patients with aortic stenosis, without coronary artery disease were included. It was demonstrated that the existence of myocardial ischemic, induced by atrial pacing and manifested by ST segment depression, had direct association to increased myocardial mass, and it had no relation with left ventricular telediastolic pressure nor with transvalvular gradient. The results support the hypothesis that an inappropriate increment of the myocardial mass is the main cause of myocardial ischemia in these type of cardiopathies.

Adolescent↗
PubMedDate not supplied

[Pacemaker activation by muscular movement].

In recent years impressive progress was achieved in the field of cardiac stimulation. Sometimes atrial systole is not available to increase stroke volume in patients with pacemakers for complete atrioventricular block. We describe a new model of heart pacemaker (Activitrax), which is activated by muscle movement and is responsive to metabolic demands, increasing the pacemaker's firing rate according to exercise. The result which allowed a better quality of life was highly satisfactory.

Adult↗
PubMedDate not supplied

[Methodology for the implantation of definitive cardiac pacemakers].

Recent technological improvements in the field of artificial cardiac stimulation have markedly increased the complexities involved in the implantation of cardiac devices. The main purpose of this article is to review the current methodology for implantation of permanent pacemakers. Standardized terminology of the ICHD for the correct identification of permanent pacemakers, indications for their installation and surgical procedures are reviewed. The authors express their personal experiences on the optimal criteria for the selection and use of the pacemakers and comment on the potential problems and complications associated with their use as well as a description of the details of device implantation. Finally, the moral and ethical considerations involved with the prescription and usage of these devices in our country are discussed.

Humans↗
PubMedDate not supplied

[Myocardial ischemia in hypertension heart disease (author's transl)].

Seventeen hypertensive patients with EKG evidence of left ventricular hypertrophy and subendocardial ischemia were studied. The following tests were performed: cine-ventriculography, coronary arteriography, ejection fraction, ventricular pressures, left ventricular mass, EKG stress test and atrial stimulation. In 10 cases cardiac scintigraphy with intracoronary injection of albumin-macro-aggregates marked with TC 99m, was obtained. EKG stress and atrial stimulation tests were positive in all cases, with ST depression greater than 1mm, or accentuation of previous ST depression. 83.7% of the patients had permeable coronary arteries, with "corkscrew' tortuosity. Left ventricular mass was increased in all cases (119 +/- 28.5% m2 s/c). Ejection fraction (74.2 +/- 8.1), and left ventricular diastolic pressures were normal. Cardiac scintigraphy showed uniform distribution of the radioisotope in the right ventricle and poor concentration with better dispersion and distribution in the left ventricle. It is concluded that subendocardial ischemia in these subjects is not produced by obstruction of the main coronary trunks and is associated to a significant increment of left ventricular mass which possibly produce a poor coronary reserve, and a potentially high risk condition.

Adult↗
PubMedDate not supplied

[Hemodynamic study in hypertensive cardiopathy under ischemia induced by atrial stimulation in the absence of fixed coronary obstructions].

With the purpose to study the haemodynamic changes that occur with myocardial ischaemia induced by atrial pacing (AP) in hypertensive heart disease, we studied 7 patients with such condition, all of them with a long time history of systemic hypertension, electrocardiographic signs at rest of left ventricular hypertrophy and ST-segment depression, at least of 0.5 mm. All the patients showed normal coronary arteries in angiocardiogram. AP was started 10 beats above the basal heart rate with increments of 10 beats every 2 minutes until a ST-segment depression at least of 2 mm was obtained which occurred in all the cases studied. After every 2 minutes of AP a simultaneous 12-leads electrocardiogram recording and left ventricular and aortic pull-back pressure were obtained. At the desired end point the AP was abruptly stopped and the same parameters were registered at 3, 5, 10 and 15 minutes until recovery. During AP the left ventricular systolic pressure (LVSP) did not show any significant change, with the exception of a patient who experienced angor pectoris during the proceeding. The left ventricular end-diastolic pressure (LVEDP) increased in 3.4 +/- 1.7 mmHg, change that was statistically significant (p less than or equal to 0.01) but not hemodynamically important since only in one patient it increased above the normal levels (from 13 mmHg basal to 17 mmHg during AP). In contrast, LVEDP markedly rose above normal when AP was stopped. It is concluded that neither LVEDP nor LVSP play an important role in the genesis of the ST segment depression seen in these patients. It is showed that, similar as in patients with obstructive coronariopathy, these cases work on a depressed Starling curve during AP and its recovery for what is thought that the functional meaning of ischaemia for both entities is similar no matter that their pathogenetic mechanisms are different.

Blood Pressure↗
PubMedDate not supplied

[Coronary circulation in asymmetrical hypertrophy of the interventricular septum. On a new pathogenic hypothesis].

Thirty-four patients with left ventricular hypertrophy were studied. In all cases the following parameters were analyzed: 1) Echocardiography:left ventricular diastolic and systolic diameters, ejection fraction, thickness and movement of interventricular septum and posterior wall of the left ventricle (LV) 2) Electrocardiography: R wave voltaje in precordial leads V2, V3 and V5 and electrical axis in frontal plane 3) Catheterization: intracavitary pressures in LV and aortic pressures 4) Left ventriculography: areas of altered contractility 5) Coronariography: distribution pattern of coronary arteries and number of first order branches of circumflex (CA) and anterior descending coronary arteries (ADCA). The population was divided into 2 groups. Group A (GA) was made up of 22 patients with concentric hypertrophy (CH) of the LV (15 with systemic hypertensive heart disease, 6 with aortic valvular stenosis and 1 idiopathic). Echocardiographic findings included posterior wall thickness (PWT) or septal thickness of 1.1. cm or more and interventricular septum-posterior wall thickness ratio (S/PW) of less than 1.3. Group B (GB) included 12 patients with asymmetric septal hypertrophy (ASH), idiopathic in 5, systemic hypertensive heart disease in 4 and aortic valvular stenosis in 3. In these patients the S/PW thickness ratio was greater than 1.3 and the thickness of either wall greater than 1.1. cm. When the data of the two groups were compared there were significant differences in relation to the presence of septal hypertrophy. The R wave voltage in V2, interventricular thickness and S/PW were greater in GB. In addition, septal movement was less in GB than in Group A (0.47 +/- 0.26 cm vs. 0.74 +/- 0.37 cm; P less than 0.05). PWT was also less in Group B than in A (B: 1.01 +/- 0.1 cm, A: 1.2 +/- 0.2 cm; P less than 0.001). The CA in Group B divided into fewer than 4 first order branches to the upper two thirds of the posterior and lateral walls of the LV in 91.6%. This distribution of circumflex branches was found in 31.8% of the patients in Group A (P less than 0.05). In Group B, the ADCA divided into septal branches with no more than 2 diagonal branches. The posterior descending artery dominated septal distribution in 100% of these cases (GA: 31.8%; P less than 0.05). The sum of the first order branches of the CA and the ADCA was 5.6 +/- 0.9 in Group A and 2.7 +/- 0.9 branches in Group B (P less than 0.01).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMedDate not supplied

[Acute electrocardiographic effects of minoxidil in hypertensive subjects].

Unexplained ST-T segment (ST-TD) or T wave depressions (TWD) in the electrocardiogram (EKG) are seen during minoxidil therapy. To study the possible cause of this phenomenon 69 essential systemic hypertensive patients were evaluated. At the 5th day of a double therapy (DT) period consisting in the administration of atenolol 100 mg/day and chlorthalidone 50 mg/day systolic blood pressure (SBP), Sokoloff Index (SI) (EKG: Svl + Rv5-v6), EST-T (sum of ST-TD and TWD areas in 9 derivations of EKG) and potassium (K) serum levels were determined. Minoxidil (10 mg/day) was added and 3 to 6 days after, all parameters were repeated. Patients were classified in group A: (GA, n25 =) or B: (GB, n = 44) at the end of the study according to the absence or presence of ST-TD or TWD, respectively. During DT, SBP and SI were lower in GA (145.3 +/- 20.9 mm of Hg and 23.8 +/- 7.5 mm, respectively): (all values in X and S) than GB (173.5 +/- 24.4 and 34.0 +/- 8.3 respectively) (p less than 0.001 for both values) delta SBP (X and S of changes at the end of the study) diminished more in GB (-40.7 +/- 22.2 mm of Hg, p less than 0001) than in GA (-20.1 +/- 15.0, p less than 0.001) (GB-GA p less than 0.001). Correlation coefficient of SBP -delta SBP in both groups and delta SBP-delta EST-T in GB was 0.75 and 0.66 (p less than 0.001 for both values) respectively. delta K was not significant. Twenty five out of 27 patients of GB didn't have stenotic lesions by coronariography. Minoxidil induced ST-TD or TWD may be due to a fall in coronary perfusion pressure in patients with left ventricular hypertrophy and poor coronary circulatory reserve. This hipothesis implies that coronary autoregulation is lost in this stage of disease.

Blood Pressure↗
PubMedDate not supplied

[Comparison between the treadmill exercise test and atrial stimulation with measurements of plasma catecholamines in patients with angina pectoris].

The assessment of atrial pacing (AP), in relation to the electrocardiographic treadmill test (ETT), was carried out in 22 patients with angina pectoris in whom the importance of the adrenergic system was also evaluated. Coronary cineangiography, left ventricular angiography and plasmatic catecholamine determinations were carried out before and after ETT and transvenous AP. All patients with coronary artery obstruction of more than 80% had positive ETT (X2 = 5.2) and 61.5% had positive AP tests (X2 = 5.2) and 61.5% had positive AP tests (X2 = 3.16). Sixty six of those patients without angiographic coronary obstruction had positive ETT and in 55.6% the AP test was also positive. The increase in systolic blood pressure was found to correlate with the increase in plasmatic catecholamine concentrations during ETT but not with AP (p less than 0.001). The electrocardiographic treadmill test has a greater specificity and sensitivity than AP and correlates with the plasmatic catecholamine concentration. Our results suggest that the myocardial ischemia produced by AP is not related to the endogenous output of catecholamines nor to the elevation of blood pressure, but rather it seems to be dependent of a greater imbalance between the cardiac debit supply ratio of oxygen induced exclusively by an increase in heart rate.

Adult↗
PubMedDate not supplied

[Prinzmetal's angina. Response to the treatment with reserpine. Review of its physiopathological mechanisms].

A case of Prinzmetal angina refractory to classic medical treatment, in which the angina attacks were suppressed with the administration qf reserpine is presented. The possible physiopathologic mecanisms of this entity are reviewed. The possibility of coronary spasm due to an alteration in the regulation of the coronary arterial tone from an autonomic.nervous system illness is established, an abnormal coronary vascular reactivity is also reviewed. It is emphasized that the Prinzmetal angina is an original entity, idfferent from the coronary arteriosclerotic heart disease, which may coexist with it but which cannot be treated in the same way, because its physiopathologic mecanisms are different.

Angina Pectoris↗