Sport modality affects bradycardia level and its mechanisms of control in professional athletes.

We investigated the influence of sport modalities in resting bradycardia and its mechanisms of control in highly trained athletes. In addition, the relationships between bradycardia mechanisms and cardiac structural adaptations were tested. Professional male athletes (13 runners, 11 cyclists) were evaluated. Heart rate (HR) was recorded at rest on beat-to-beat basis (ECG). Selective pharmacological blockade was performed with atropine and esmolol. Vagal effect, intrinsic heart rate (IHR), parasympathetic (n) and sympathetic (m) modulations, autonomic influence (AI) and autonomic balance (Abal) were calculated. Plasmatic norepinephrine (high-pressure liquid chromatography) and cardiac structural adaptations (echocardiography) were evaluated. Runners presented lower resting HR, higher vagal effect, parasympathetic modulation (n), AI and IHR than cyclists (P<0.05). Abal, sympathetic modulation (m) and norepinephrine level were similar within athletes regardless of modality. The cardiac chambers were also similar between runners and cyclists (P=0.30). However, cyclists displayed higher septum and posterior wall thickness than runners (P=0.04). Further analysis showed a trend towards inverse correlation between IHR with septum wall thickness and posterior wall thickness (P=0.056). Type of sport influences the resting bradycardia level and its mechanisms of control in professional athletes. Resting bradycardia in runners is mainly dependent on an autonomic mechanism. In contrast, a cyclist's resting bradycardia relies on a non-autonomic mechanism probably associated with combined eccentric and concentric hypertrophy.

Comparison of risk of orthostatic hypotension in elderly depressed hypertensive women treated with nortriptyline and thiazides versus elderly depressed normotensive women treated with nortriptyline.

This is a nonblind, case-controlled study comparing the risk of orthostatic hypotension (OH) in 2 groups of elderly depressed women: 22 normotensive and 21 hypertensive patients receiving thiazides. Blood pressure measurements and tilt-table tests produced similar results: increased drop in systolic blood pressure (SBP) after standing (p <0.001), with no significant differences between the groups (p = 0.523). There were no changes on diastolic blood pressure (DBP) after standing, or in SBP or DBP at rest. Dizziness was reported by 23 subjects (53.5%) before treatment, and by 16 subjects (38.1%) at week 8. Complaints of dizziness were not associated with OH (Kappa = 0.07).

[Myocardial dysfunction secondary to persistent tachycardia]. / Disfunção miocárdica secundária à taquicardia persistente.

This study demonstrates the presence of variable degrees of reversible ventricular dysfunction in five patients with incessant atrioventricular tachycardia (IAVT) submitted to surgical ablation of the anomalous pathway. The patients were three females and two males, with age ranging from four to 39 years (mean 15.2). Preoperative EKG presented persistent tachycardia with narrow QRS and RP greater than PR in every case. The P wave was negative in leads D2, D3, AVF from V2 to V6. The 24 hours Holter monitoring demonstrated IAVT rhythm with few sinus beats. The heart rate variated from 140 to 190 bpm (mean 158 bpm). The echocardiogram ejection fraction ranged from 33% to 59% (mean 49.6%). The left ventricular diastolic diameter varied from 47 to 66 mm (mean 53.8). The chest X-ray showed moderate heart enlargement in two patients and mild enlargement in one. All the patients were refractory to isolated or associated antiarrhythmic drugs. Postero-septal anomalous A-V pathway (with exclusively slow retrograde conduction, was demonstrated by electrophysiologic study. After surgery every patient was asymptomatic without medication. Permanent sinus rhythm with heart rate of 62 to 100 bpm (mean 78.4 bpm) in a four months to two years follow-up. The postoperative echocardiogram ejection fraction ranged from 63% to 81% (mean 71.6%) and the left ventricular diastolic diameter was 42 to 57 mm (mean 48.2 mm). The heart area was normal in four patients and mildly increased in one patient. Thus, persistent increase in heart rate induces variable degrees of reversible myocardial dysfunction.