Neurocardiology has many dimensions, but it may be conceptualized as divided into 3 major categories: the heart’s effects on the brain (eg, cardiac source embolic stroke), the brain’s effects on the heart (eg, neurogenic heart disease), and neurocardiac syndromes (eg, Friedreich disease). The present review deals with the nervous system’s capacity to injure the heart. This subject is inherently important but also represents an example of a much more widespread and conceptually fascinating area of neurovisceral damage in general.

In 1942, at the culmination of his distinguished career as Professor of Physiology at Harvard Medical School, Walter B. Cannon published a remarkable paper entitled “‘Voodoo’ Death,”1 in which he recounted anecdotal experiences, largely from the anthropology literature, of death from fright. These often remote events, drawn from widely disparate parts of the world, had several features in common. They were all induced by an absolute belief that an external force, such as a wizard or medicine man, could, at will, cause demise and that the victim himself had no power to alter this course. This perceived lack of control over a powerful external force is the sine qua non for all the cases recounted by Cannon, who postulated that death was caused “by a lasting and intense action of the sympathico-adrenal system.” Cannon believed that this phenomenon was limited to societies in which the people were “so superstitious, so ignorant, that they feel themselves bewildered strangers in a hostile world. Instead of knowledge, they have fertile and unrestricted imaginations which fill their environment with all manner of evil spirits capable of affecting their lives disastrously.” Over the years since Cannon’s observations, evidence has accumulated to support his concept that “voodoo” death is, in fact, a real phenomenon but, far from being limited to ancient peoples, may be a basic …

The Brain–Heart Connection

Propofol infusion syn- drome (PRIS) is a rare and often fa- tal syndrome described in critically ill children undergoing long-term propofol infusion at high doses. Re- cently several cases have been re- ported in adults, too. The main fea- tures of the syndrome consist of car- diac failure, rhabdomyolysis, severe metabolic acidosis and renal failure. To date 21 paediatric cases and 14 adult cases have been described. These latter were mostly patients with acute neurological illnesses or acute inflammatory diseases compli- cated by severe infections or even sepsis, and receiving catecholamines

http://link.springer.com/content/pdf/10.1007/s00134-003-1905-x.pdf

The pathophysiology of propofol infusion syndrome: a simple name for a complex

Propofol infusion syndrome (PRIS) is a rare and often fatal syndrome described in critically ill children undergoing long-term propofol infusion at high doses. Recently several cases have been reported in adults, too. The main features of the syndrome consist of cardiac failure, rhabdomyolysis, severe metabolic acidosis and renal failure. To date 21 paediatric cases and 14 adult cases have been described. These latter were mostly patients with acute neurological illnesses or acute inflammatory diseases complicated by severe infections or even sepsis, and receiving catecholamines and/or steroids in addition to propofol. Central nervous system activation with production of catecholamines and glucocorticoids, and systemic inflammation with cytokine production are priming factors for cardiac and peripheral muscle dysfunction. High-dose propofol, but also supportive treatments with catecholamines and corticosteroids, act as triggering factors. At the subcellular level, propofol impairs free fatty acid utilisation and mitochondrial activity. Imbalance between energy demand and utilisation is a key pathogenetic mechanism, which may lead to cardiac and peripheral muscle necrosis.

The pathophysiology of propofol infusion syndrome: a simple name for a complex syndrome

Experimental catecholamine-induced myocardial necrosis I. morphology, quantification and regional distribution of acute contraction band lesions

Electrocardiographic abnormalities have been known to occur in the context of neurologic disease for a long time. These changes fall into 2 categories: arrhythmias and repolarization abnormalities. However, until relatively recently these changes were believed to represent purely electrophysiologic alterations and not real heart disease. It is now clear that some patients with neurogenic electrocardiographic changes show cardiac enzyme release and myofibrillar degeneration at autopsy. There are 4 major methods for producing myofibrillar degeneration (i.e., contraction band necrosis or coagulative myocytolysis): catecholamine infusion, stress-steroid, nervous system stimulation and reperfusion. The common thread connecting these 4 methods is the opening of receptor-operated calcium channels, resulting in intense contraction of cardiac muscle. Thus, neurogenic influence over cardiac function may represent a continuum. In the mild reversible circumstance, only the electrocardiographic change will be seen, whereas in the severe, irreversible situation, myofibrillar degeneration will ensue with release of cardiac enzymes. Cardiac cell death may be caused by oxygen free radicals produced by metabolism of catecholamines or reperfusion or both, after variable periods of ischemia. This concept represents a unifying hypothesis, tying together the clinical, physiologic, biochemical and pathologic findings in neurogenic heart disease.

Neurogenic heart disease: A unifying hypothesis

The evolutive histological stages, the frequency, and the eventual association of the different types of myocardial cell death have been studied in the following human material: acute infarction, sudden "coronary" death, accidental death, pheochromocytoma, transplanted hearts, "stone" heart syndrome, thrombotic thrombocytopenic purpura, and alcoholic cardiomyopathy. Three distinct main histological types of myocardial cell death are recognizable: Coagulation necrosis, the fundamental lesion in infarcts in which the myocardial cell loses its capability to contract and dies in an atonic state with overdistension due to the intraventricular pressure. No early myofibrillar damage is seen. Coagulative myocytolysis, found in all the present cases, always seen in the outer zone of an early infarct and in the surrounding normal myocardium at any stage of the repair process in most of the acute infarcts and in most cases of sudden death. The myocardial cell dies in a hypercontracted state, with early myofibrillar rhexis, and anomalous irregular cross-band formations. This tetanic death is similar to that seen in pheochromocytoma and in experimental catecholamine-induced necrosis. Colliquative myocytolysis, in which edematous vacuolization with dissolution of myofibrils is the main early finding, without hypercontraction, anomalous bands, and myofibrillar rhexis. This pattern, likely related to the low-output syndrome, was often seen in the preserved subendocardial and perivascular muscle fibers of acute infarct cases, in some transplanted hearts, and in all the alcoholic hearts. The different clear-cut morphological patterns of these three types of myocardial necrosis suggest a different pathogenesis and that different pathogenetic mechanisms may act in the same disease.

Different morphological types of myocardial cell death in man.

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Different morphological types of myocardial cell death in man.