Transient global amnesia as a manifestation of acute myocardial infarction: a case of missed sudden cardiac death?

Acute myocardial infarction may lead to several clinical manifestations and many times this diagnosis is missed. Transient global amnesia (TGA) is a well-defined clinical syndrome of unknown etiology. Several mechanisms have been proposed but only trigger events have been clearly associated with the attack. We describe a case of acute myocardial infarction manifestated by TGA.     

Is a functional sarcoplasmic reticulum necessary for preconditioning?

Several studies have shown that the protective effect of ischemic preconditioning (PC) is associated with decreased calcium release from the sarcoplasmic reticulum (SR). However, no study has yet demonstrated whether these changes are essential in the mechanism of PC. In order to investigate whether a functional SR was necessary for PC, we manipulated SR calcium handling using (i) 0.1microM ryanodine (RY), a concentration known to lock the SR calcium release channel in the open state and (ii) 50microM cyclopiazonic acid (CPA), a specific inhibitor of the SR calcium ATPase. Initial experiments confirmed that both RY and CPA eliminated the ability of the SR to accumulate calcium. Isolated rat hearts (n=6-7/group) were perfused normoxically for 30 min prior to either a further 40 min of perfusion [control (C)] or 4x[5 min ischemia (I) + 5 min reperfusion (R)] (PC). All hearts were then subjected to a further 40 min I + 40 min R. The C and PC protocols were then repeated in the presence of RY or CPA, introduced after 10 min of perfusion.(31)P-NMR was used to measure ATP, PCr, P(i)and intracellular pH. RY and CPA decreased developed pressure (DP) by 75% and 59%, respectively. Percentage recovery of LVDP was significantly higher in PC (72+/-8%), PC+RY (72+/-7%) and PC+CPA (49+/-7%) groups compared with their respective controls (43+/-7%, 47+/-7% and 10+/-4%) (P<0.05). Thus, PC remains protective in the presence of a SR unable to accumulate calcium, suggesting that the changes in SR calcium release are not essential in the mechanism of preconditioning.     

Defibrillators--end of sudden cardiac death?

The ventricular fibrillation is still the main cause of a sudden cardiac death, even though it was described 155 years ago in experiment (M. Hoffa 1849) and its therapy--defibrillation--has been known since 1947 (C. Beck). In Europe 2500 inhabitants suffer from cardiac arrest daily and 90% is caused by ventricular fibrillation. A key interval for an effective defibrillation seems to be 3-8 minutes from the begining of a cardiac arrest. Automated (automatized) external defibrillators (AED) have been used for last 15 years, especially in USA. However it is still unclear how many devices will be needed and where to place them. We don't know if they improve the prognosis of patients with out of hospital cardiac arrest during ventricular fibrillation. The individualisation of the risk of a sudden cardiac death has brought a new method to the clinical practise--implantation of cardioverter-defibrillator (ICD). Their efficacy in reduction of total mortality was verified first in the field of secondary prevention--in patients after cardiac arrest (AVID study) and than in the field of primary prevention--in patients with risk markers (left ventricle dysfunction, non sustained ventricular tachycardias) but without sustained malignant arrhythmia in anamnesis (MUSTT, CIDS, MADIT I, MADIT II). Defibrillators (external, automated, implantable) obviously don't mean the end of the sudden cardiac death. The incidence of sudden cardiac death can be reduced significantly with prevention (nutrition, prevention of CAD) and one attention should be drawn to the fact even in the future.     

Effect of tachycardia on myocardial sarcoplasmic reticulum and Ca2+ dynamics: a mechanism for preconditioning?

We have previously demonstrated that brief episodes of tachycardia prior to a prolonged occlusion of a coronary artery, followed by reperfusion, substantially reduce the infarct size. Adenosine receptors and mitochondrial ATP-dependent K(+) channels mediate this effect. Since preconditioning can be induced or reverted by maneuvers that increase or decrease [Ca(2+)](i), respectively, and tachycardia increases [Ca(2+)](i), we studied the participation of sarcoplasmic reticulum and Ca(2+) in the preconditioning effect of tachycardia. We measured the effect of ischemia and tachycardia on Ca(2+) uptake and release by sarcoplasmic reticulum vesicles isolated from left ventricular canine myocardium. Myocardial ischemia increased Ca(2+)-release rate constants and decreased both the initial rates of Ca(2+) uptake and [(3)H]-ryanodine binding by sarcoplasmic reticulum. In addition, ischemia induced a decrease in the pentameric form of phospholamban and in the content of ryanodine-receptor Ca(2+)-release channel protein. All these effects were reverted in hearts preconditioned with tachycardia. Furthermore, tachycardia by itself increased [(3)H]-ryanodine binding, Ca(2+)-release rate constants and the protein levels of ryanodine-receptor Ca(2+)-release channels and the ATP-dependent Ca(2+) pump. These results suggest that tachycardia preserves the integrity of the sarcoplasmic reticulum preventing the excess of release and the decrease of uptake of Ca(2+) produced by ischemia, thereby avoiding cytosolic Ca(2+) overload. This sarcoplasmic reticulum protection could partly explain the preconditioning effect of tachycardia.     

Cardiac angiosarcoma: too little known, too late treatment or just too bad a tumour?

Cardiac angiosarcoma is a rare tumour. Current imaging techniques (magnetic resonance imaging, MRI; computed axial tomography, CAT; 2-D echocardiography), although useful in delineating the extent of tumour involvement, do not correlate well with intraoperative findings of resectability. We report a case were palliative surgical resection was technically possible, contrary to expectations from CAT and MRI findings. However, the patient was clinically in extremis, with advanced ventricular dysfunction, and died. Despite the short-term risk involved in surgery, if palliative resection is possible, a multidisciplinary approach with adjuvant chemotherapy and radiation can result in mid-term survival.     

Implanted defibrillators and primary prevention of sudden cardiac death: where are we today?

Implanted defibrillators have become a mainstream therapy for the prevention of sudden cardiac death (SCD) from ventricular tachyarrhythmias in patients with chronic coronary artery disease. A decade of studies has confirmed the superiority of ICDs over antiarrhythmic drug therapy in prolonging the life of patients with a prior history of sustained VT or VF. Furthermore, recent studies have examined the role of ICD therapy in the primary prophylaxis against sudden death in patients considered at high risk for ventricular tachyarrhythmias. These studies have revealed that in selected patients with the substrate of chronic coronary artery disease and a ventricular scar, ICDs lead to important relative and absolute reductions in mortality in such patients without a prior history of VT or VF. Clinicians caring for patients with chronic coronary artery disease (CAD) and severe LV dysfunction, who are at a risk of sudden cardiac death, need to carefully consider this information when managing this patient population.