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Enhanced transcardiac l-norepinephrine response during cold pressor test in obstructive coronary artery disease
Insights
Patients with obstructive coronary artery disease show enhanced cardiac norepinephrine release during cold stress. This heightened sympathetic response may increase the risk of acute cardiac events.
Area of Science:
- Cardiology
- Neuroscience
- Physiology
Background:
- Increased cardiac sympathetic activity affects coronary vasomotor tone and can lower the ventricular fibrillation threshold.
- Understanding myocardial responses to sympathetic stimulation is crucial for assessing cardiac event risk.
Purpose of the Study:
- To compare transcardiac l-norepinephrine responses to cold pressor testing in patients with normal coronary arteries versus those with obstructive coronary artery disease.
- To investigate potential differences in myocardial norepinephrine release under sympathetic stress between these groups.
Main Methods:
- Compared 20 patients with normal coronary arteries and 23 with obstructive coronary artery disease.
- Utilized the cold pressor test to induce sympathetic stimulation.
- Measured arterial and coronary sinus l-norepinephrine levels to assess transcardiac responses.
Main Results:
- Baseline hemodynamic data were similar, except for higher left ventricular end-diastolic pressures in the coronary artery disease group.
- Cold stimulus induced similar hemodynamic responses in both groups.
- Patients with coronary artery disease demonstrated a significantly greater increase in coronary sinus norepinephrine compared to arterial norepinephrine, indicating net myocardial release (p < 0.02).
Conclusions:
- Transcardiac l-norepinephrine responses are enhanced during cold stimulus in patients with obstructive coronary artery disease.
- This exaggerated myocardial norepinephrine release during sympathetic stress may contribute to an increased risk of acute cardiac events.
Abstract:
An increase in cardiac sympathetic activity can enhance coronary vasomotor tone and lower the ventricular fibrillation threshold. We compared the transcardiac l-norepinephrine responses during cold pressor test of 20 patients with normal coronary arteries with those of 23 patients with obstructive coronary artery disease. Baseline hemodynamic data did not differ in the 2 patient groups except for left ventricular end-diastolic pressures; mean values (+/- standard deviation [SD] were 10 +/- 3.7 and 15 +/- 4.5 mm Hg in patients with normal and abnormal coronary arteries (p less than 0.01). Baseline l-norepinephrine contents averaged 295 +/- 152 (normal coronary arteries) and 250 +/- 134 pg/ml (coronary artery disease) in the arterial blood, and 273 +/- 152 and 250 +/- 115 pg/ml, respectively, in the coronary sinus blood. Hemodynamic responses during cold stimulus were similar in both groups. Also, cold pressor-induced increases in arterial and coronary sinus l-norepinephrine contents were balanced in patients with normal coronary arteries, averaging 19 +/- 30 and 17 +/- 37%, respectively. In patients with coronary artery disease, however, a 26 +/- 58% increase in arterial l-norepinephrine contents was associated with a 58 +/- 62% increase in coronary sinus l-norepinephrine contents (p less than 0.02), suggesting myocardial l-norepinephrine net release. It is concluded that transcardiac l-norepinephrine responses during cold stimulus are enhanced in patients with obstructive coronary artery disease. This response to a relatively mild sympathetic stress, reproducible by a variety of analogous stressful situations during daily life, could present an increased risk for acute cardiac events.