SUMMARConventional doctrine states that the QT interval is related to heart rate in an inverse exponential relationship, so that with increasing rate the QT interval shortens. This relationship has recently been studied in a group of patients undergoing physiological exercise stress tests, atrial pacing stress test, and in a further group of patients with complete heart block undergoing exercise at a fixed ventricular rate controlled by cardiac pacemaker. Examinations of recordings made during physiological exercise do show the expected shortening in QT interval, we believe that this shortening is only in part due to the intrinsic effect of increased rate as patients who were atrially paced to similar rates and within the same age group showed only a small decrease in measured QT interval and patients undergoing exercise at fixed ventricular rate showed shortening in QT interval which was related to the independent atrial rate. It appears, therefore, that the QT interval is governed mainly by extrinsic factors and not intrinsically rate related.The physiological control of QT interval is being used now to construct a cardiac pacemaker which senses the interval between the delivered stimulus and the evoked T wave so that the stimulus-evoked T wave interval could be used to set the subsequent escape interval and subsequently the overall pacing rate. Physiological control of cardiac pacing rate using conventional unipolar lead systems and independent of atrial activity is possible and currently being investigated.
Additional Indexing Words: Corrected QT intervalControl of cardiac pacemaker Catecholamines B AZETT1) in 1920 first described a non-linear relationship between the QT interval and the heart rate which has been widely applied to derive the rate corrected QT interval (QTc). Roy et al2) in 1976 reported that in a subject with familial prolongation of the QT interval the QTc actually prolonges with increasing rate during
Traditionally, clinical conditions synonymous with the ageing male included cardiovascular disease (CVD), type 2 diabetes mellitus (DM) and sexual dysfunction, and were widely regarded as independent clinical entities. Over the last decade, interrelationship of clinical conditions has been convincingly demonstrated. Declining testosterone levels in the elderly, once regarded as an academic endocrinological question, appear to be central to the listed pathologies. It is now clear that erectile dysfunction is an expression of endothelial dysfunction. Testosterone deficiency is associated with an increased incidence of CVD and DM. The latter is often the sequel of the metabolic syndrome. Visceral obesity, a pivotal characteristic of the metabolic syndrome, suppresses the hypothalamic-pituitary-testicular axis leading to diminished testosterone production. Conversely, substantial androgen deficiency leads to signs and symptoms of metabolic syndrome. It is erroneous not to include testosterone measurements in the progress of the CVD, DM and erectile dysfunction. These conditions correlate strongly with testosterone deficiency.
We studied 124 homosexual men aged 36.7 +/- 7.6 years (range 23-57) using Doppler echocardiography. One hundred and one patients (Group A) had had acquired immunodeficiency syndrome for 1.6 +/- 1.0 years and 23 patients (Group B) had had HIV infection without opportunistic infections for 3.2 +/- 2.3 years. Doppler echocardiography was normal in 31% of Group A patients and in 61% of Group B. Pericardial effusion was found in 44 Group A patients (44%) and two Group B patients (9%). In Group A, left ventricular dilatation and/or dysfunction were found in 20 patients (20%), aortic root dilatation and regurgitation in eight patients (8%) and an intracardiac echogenic mass in seven patients (7%); in Group B one patient (4%) had an intracardiac mass. Forty-four (44%) Group A patients had cardiac presentations, and of these 22 had cardiomegaly with clinical signs of heart failure; 10 patients had tachyarrhythmias compared to only two in Group B. Although the CD4 lymphocyte count (%) was significantly lower in Group A than in Group B (5.4 +/- 6.1 vs 13.3 +/- 7.3, P < 0.001), the presence of pericardial effusion, left ventricular dysfunction, right-sided cardiac enlargement or the duration of HIV infection, did not relate to the CD4 level in either group. Although often not diagnosed clinically, cardiac involvement in patients with AIDS is a clinical reality, with pericardial effusion, cardiomyopathy and left ventricular dysfunction appearing to have a high prevalence in male homosexual patients with AIDS. These clinical and echocardiographic findings are associated with clinically apparent intercurrent opportunistic infections, rather than the HIV virus per se, or the severity of infection as reflected by the CD4 count.
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