Hanna Wachowiak-Baszyńska

Shortening baroreflex delay in hypertrophic cardiomyopathy patients -- an unknown effect of β-blockers.

AIMS Hypertrophic cardiomyopathy (HCM) is characterized by left ventricular hypertrophy and impaired diastolic and systolic function. Abnormal sympathetic-parasympathetic balance is a potential stimulus for left ventricular hypertrophy in HCM patients. β-Blockers are routinely used in HCM for their strong negative inotropic effect; however, these drugs also influence the sympathetic-parasympathetic balance. This study aimed to determine the autonomic control of the cardiovascular system and the autonomic effects of β-blockers in HCM patients treated or untreated with β-blockers. METHODS Among 51 HCM outpatients (18-70 years old; 29 men) there were 19 individuals with no medication and 32 subjects treated with a β-blocker. Fourteen age- and gender-matched (23-70 years old; nine men) healthy volunteers were enrolled in the control group. Continuous, non-invasive finger blood pressure was recorded during supine rest for 30 min. Autonomic regulation of the cardiovascular system was measured by heart rate variability and spontaneous baroreflex function (cross-correlation sequence method). RESULTS The mean pulse interval, time domain and spectral measures of heart rate variability and baroreflex sensitivity were comparable between HCM patients, treated or not with β-blockers, and the control group. However, the delay of the baroreflex was significantly longer in HCM patients who were not treated with β-blockers [2.0 (1.6-2.3) s] in comparison with HCM patients receiving β-blockers [1.4 (1.1-1.8) s; P = 0.0072] or control subjects [1.2 (0.8-1.8) s; P = 0.0025]. This delay did not differ between HCM patients treated with β-blockers and the control group. CONCLUSIONS Hypertrophic cardiomyopathy not treated with β-blockers is accompanied by prolonged baroreflex delay. The use of β-blockers normalizes this delay.

Dynamic variability of T wave polarity in 12-lead ambulatory ECG as a sign of imminent hypertrophic cardiomyopathy.

A 27-year-old male had suffered from eight episodes of exercise-induced syncope since he was seven years old. He had professionally trained for soccer and judo. His mother had died aged 46 of dilated cardiomyopathy. ECG revealed: sinus rhythm (SR), rSr’ pattern in V1, flat negative T waves in II, III, aVF, V5–V6, left ventricular hypertrophy (LVH) criteria not met. 12-lead ambulatory ECG revealed: major variability of T wave polarity, particularly in inferolateral leads; inverted T waves of various amplitude observed by day, completely normalised at night. Tilt test was negative. Echocardiography revealed: minor LVH (≤ 12 mm), normal LV function referred to as ‘athletic hypertrophy’. Exercise treadmill test (ETT) revealed: achieved predicted workload, then blood pressure (BP) drop to 90/60 mm Hg at heart rate (HR) of 180 bpm, followed by progressive HR slowing to 15 bpm with ultimate pauses (≤ 6.1 s) over next 2 min (Fig. 1). Subsequently, SR at 70 bpm and BP of 130/80 mm Hg restored. Coronary angiography revealed no abnormalities. Exercise-induced neurocardiogenic syncope was diagnosed and a dual-chamber pacemaker was implanted. Further professional training was discouraged. He remained asymptomatic for the next 4.5 years. Progressive LVH (IVS 16 mm) allowed for a diagnosis of hypertrophic non-obstructive cardiomyopathy (HNOC) and the pacemaker was upgraded to implantable cardioverter-defibrillator. Two months later, a dual-chamber pacemaker was implanted to his brother (normal resting ECG, four syncopes and Mobitz type II AV block in Holter ECG). Early hypertrophic cardiomyopathy (HCM) diagnosis and prediction of life-threatening events is still challenging and the prognostic importance of ECG-based modalities remains unclear due to their relatively low sensitivity (Baggish A et al. Heart, 2009; 95: 345–347; Erice B et al. Scand J Med Sci Sports, 2009; 19: 356–363). In this report, the diagnostic investigation initially focused on reproducing the syncopal episodes. Ambulatory ECGs and tilt test failed. However, routine ETT revealed the pathomechanism of exercise-induced syncope, allowing for implantation of a pacemaker that protected against future syncope. Nevertheless it could diminish further diagnostic alertness by documenting a neurocardiogenic cause of syncope. At that stage there was no concrete rationale for further investigation for cardiomyopathy. The subtle LVH was, at that time, being linked to the physiological hypertrophy observed in athletes. The marked T wave variability observed in 12-lead ambulatory ECG is intriguing. Negative T waves in II, III, aVF, V5–V6 in the resting ECG were qualified nonspecific. However, T wave variability, i.e. inverted T waves by day (mostly sympathetic modulation) and then normalised during night sleep (predominating parasympathetic tone) is most probably a specific ECG picture of an initial stage of HCM. Normalisation of T waves persisting at night actually excludes new myocardial ischaemia. Also, no chest pain was reported on ETT. It seems that this day-to-night dynamic variability of T wave polarity may be a distinct diagnostic sign of an early stage of HNOC that could add to a differential diagnosis with athletic LVH.

Unresectable cardiac pseudoneoplasms causing ventricular tachycardia.

Cardiac pseudoneoplasms are rare and benign. According to World Health Organization, they are classified as tumor-like lesions. We report two patients with recurrent ventricular tachycardia (VT) in whom magnetic resonance imaging revealed a pathological mass occupying a large part of the left ventricle. The localization of both tumors precluded the possibility of resection; thus, only surgical biopsy was performed. After deducting the prospect of malignancy of the tumors, we treated both patients with amiodarone and implantation of a cardioverter-defibrillator [implanted cardioverter/defibrillator (ICD)]. VT is one of many probable symptoms indicating a tumor within the heart; therefore, treatment with an ICD should only be considered after a more thorough diagnosis.