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Hemodynamic and metabolic responses to pacing in patients with chest pain and normal coronary arteriograms
Insights
Patients with chest pain and normal coronary arteriograms showed abnormal hemodynamic responses during pacing, indicating potential underlying cardiac issues. Elevated pulmonary capillary pressure and abnormal left ventricular pressures were key indicators in affected groups.
Area of Science:
- Cardiology
- Clinical Physiology
Background:
- Chest pain with normal coronary arteriograms presents a diagnostic challenge.
- Hemodynamic and metabolic assessments are crucial for evaluating cardiac function.
Purpose of the Study:
- To investigate hemodynamic and metabolic responses to atrial and coronary sinus pacing in patients with chest pain and normal coronary arteriograms.
- To differentiate patient groups based on their responses to pacing.
Main Methods:
- Evaluated 41 patients with chest pain and normal coronary arteriograms.
- Utilized atrial and coronary sinus pacing.
- Monitored hemodynamic parameters including pulmonary capillary pressure and left ventricular end-diastolic pressure.
- Assessed metabolic responses, specifically lactate production.
Main Results:
- Patients with angina, lactate production, or ST depression (group II) exhibited significantly higher pulmonary capillary pressure during peak pacing compared to normal responders (group I).
- Abnormal left ventricular end-diastolic pressure responses were observed in 6 of 9 group II patients.
- Patients with prolapsing mitral valve (group III) also showed elevated pulmonary capillary pressure, with a significantly lower stroke index during peak pacing.
- Lactate production was common in group II, but less so in group III, suggesting distinct pain mechanisms.
Conclusions:
- Pacing can reveal abnormal hemodynamic and metabolic responses in patients with chest pain and normal coronary arteriograms.
- Elevated pulmonary capillary pressure and abnormal left ventricular pressures during pacing are indicative of underlying cardiac dysfunction.
- Distinct responses in patients with angina versus mitral valve prolapse suggest different pathophysiological mechanisms for chest pain.
Abstract:
Hemodynamic and metabolic responses to pacing from either the coronary sinus or right atrium were evaluated in 41 patients with chest pain and normal coronary arteriograms. A group of patients (group II) with angina, lactate production, or significant ST segment depression had a significantly higher mean pulmonary capillary pressure on peak pacing or angina than did a group of patients considered to have a normal pacing response (group I). In 6 of 9 group II patients, the left ventricular end-diastolic pressure either rose abnormally with pacing or was greater than 14 mm Hg immediately after pacing and resembled that of a group of patients with coronary artery disease; Patients with a prolapsing mitral valve (group III) also had a significantly higher pulmonary capillary pressure on peak pacing as compared to those of group I, although abnormal left ventricular pressure responses occurred in only 2 of 9 of these patients. The stroke index was significantly lower in group III on peak pacing while group II was no different from group I. Lactate production occurred in 6 of 9 group II patients. However, only 1 of 6 patients with a prolapsing mitral valve who were studied for lactate production was found to produce lactate, suggesting a different mechanism for their pain.
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