Although several repair mechanisms have been described in the human heart, all fall too short to prevent clinical heart disease in most acute or chronic pathological cardiac conditions. Moreover, despite many breakthroughs in cardiovascular medicine, the complications of a myocardial infarction such as chronic heart failure remains a serious worldwide problem. Bone marrow stem cells could provide for a promising strategy to restore myocardial infarctions and prevent postinfarct congestive heart failure, because there is growing body of evidence that bone marrow stem cells, such as mesenchymal stem cells, can generate new cardiomyocytes in animals and humans. In this review, we will discuss important issues on stem cell therapy for cardiac regeneration after myocardial infarction, which might be of paramount importance when considering future human trials.

A case is reported of haemodynamic collapse in a 51 year old male heterotopic heart transplant recipient caused by native heart ventricular tachycardia. An accurate diagnosis was made by selective right and left sided electrocardiography. Synchronised electrical cardioversion of the native heart (200 J) resulted in restoration of sinus rhythm with prompt relief of symptoms and amelioration of the clinical situation. (Heart 1999;81:323-324) Keywords: transplantation; ventricular tachycardia A 51 year old man underwent heterotopic heart transplantation because of end stage ischaemic heart disease and fixed pulmonary hypertension. Two days after transplantation he was admitted to the intensive care unit because of sudden haemodynamic collapse. His clinical course had been uneventful, but he presented with cardiogenic shock characterised by hypotension (blood pressure 55/46 mm Hg), severe respiratory distress, and a rapid irregular heart rate of approximately 150 beats/min.The 12 lead ECG (fig 1) showed a broad QRS complex tachycardia with a left bundle branch block morphology at a rate of 245 beats/min. According to the standard ECG criteria 1 he was diagnosed with ventricular tachycardia; however, the exact nature of the tachycardia remained obscure as narrow QRS complexes were interposed between the broad ones in the peripheral limb leads. Although these narrow beats during ventricular tachycardia could result from capture or echo beats, they most probably reflected normal activation of the non-aVected heart. We wondered from which heart-donor or host-the arrhythmia originated. In contrast to the left precordial leads (V2-6), the precordial V1 lead showed sinus tachycardia; therefore an ECG in the dextrocardia position was taken by positioning the precordial leads rightwards on the chest. This right sided ECG showed ventricular tachycardia in V1R whereas precordial leads V2R-6R showed sinus rhythm (fig 1). As the donor heart is positioned rightward to the

Background Changes in left ventricular (LV) activation after cardiac resynchronization therapy (CRT) influence survival but are difficult to quantify noninvasively. Methods and Results We studied 527 CRT patients to assess whether noninvasive quantification of changes in LV activation, defined by change (Δ) in QRS area (QRSA), can predict outcomes after CRT. The study outcome was time until LV assist device(LVAD), cardiac transplant, or death. The three‐dimensional QRSA was measured from clinical 12 lead ECGs which were transformed into vectorcardiograms using the Kors method. QRSA was calculated as (QRSx2 + QRSy2 + QRSz2)1/2; ΔQRSA was calculated as post‐QRSA minus pre‐QRSA, where a negative value represents a reduction in LV activation delay. Kaplan–Meier plots and multivariable Cox proportional hazards models were used to relate ΔQRSA area with outcomes after stratifying the population into quartiles of ΔQRSA. The median baseline QRSA of 93.6 µVs decreased to 59.7 µVs after CRT. Progressive reductions in QRSA with CRT were associated with a lower rate of LVAD, transplant, or death across patient quartiles (P < .001). In Cox regression analyses, ΔQRSA was associated with outcomes independent of QRS morphology and other clinical variables (Q1[greatest decrease] vs Q4[smallest change=reference], HR 0.45, CI, 0.30‐0.70, P < .001). There was no interaction between ΔQRSA and QRS morphology. Conclusions CRT induced ΔQRSA was associated with clinically meaningful changes in event‐free survival. ΔQRSA may be a novel target to guide lead implantation and device optimization.