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Angina-like cardiac disturbances of hypothalamic etiology in cat, monkey, and man
Insights
Central nervous system (CNS) lesions, particularly in the hypothalamus, can induce angina-like symptoms. This research links brain activity to cardiac pain presentation without arrhythmias.
Area of Science:
- Neuroscience
- Cardiology
- Pathology
Background:
- Investigated angina-like phenomena originating from the central nervous system (CNS).
- Analyzed clinical cases involving cerebral hematoma, concussion, and tumors with associated cardiological disturbances.
- Focused on cases with angina-like symptoms and absence of ectopic beats or arrhythmias.
Observation:
- Observed cardiological disturbances secondary to compressive brain lesions or surgical interventions.
- Identified the hypothalamus as a key brain region associated with these angina-like phenomena.
- Stimulation of specific hypothalamic sites in animal models induced angina-like manifestations without other cardiac changes.
Findings:
- Confirmed a link between hypothalamic involvement and cerebrally induced angina-like syndromes.
- Hypothalamic stimulation in awake monkeys produced angina-like electrocardiogram (ECG) changes and behavior indicative of referred pain.
- Repetitive hypothalamic stimulation led to pathological myocardial changes, including bleeding and necroses, particularly with persistent ECG alterations.
Implications:
- Suggests the hypothalamus plays a critical role in mediating cardiac pain perception.
- Highlights the potential for CNS dysfunction to manifest as cardiac symptoms, mimicking angina.
- Underscores the importance of considering neurological etiologies in patients presenting with unexplained angina-like symptoms.
Abstract:
Angina-like phenomena of CNS etiology were studied. Data were collected and analyzed from clinical cases of cerebral hematoma, concussion, and tumors in which cardiological disturbances were observed consequent to compressive brain lesions or surgical brain manipulations. The cases in which the disturbances were largely angina-like and without ectopic beats or arrhythmias were chosen for study. The brain region most significantly related to this phenomenon seemed to be the hypothalamus. Experiments conducted in cats and monkeys showed that stimulation of specific sites in the hypothalamus resulted in angina-like manifestations with no other cardiac changes. These data support our working hypothesis that a cerebrally induced syndrome that is conspicuously angina-like must be related to hypothalamic involvement. In the awake monkey hypothalamic stimulation caused angina-like ECG changes and behavior suggestive of referred pain. In some cases, repetitions of the stimulations or irritations in all of the species resulted in permanent pathological myocardial changes, mostly bleeding into the myocardium. In some animals there were minute hemorrhagic necroses that were subepicardial in distribution. It is significant that the most severe or permanent pathological changes were found in cases in which the angina-like ECG alterations were persistent. There were also cases, however, with persistent angina-like ECG changes that showed no such pathology.