Prognostic Significance of Systolic Blood Pressure Changes During Dobutamine-Atropine Stress Technetium-99m Sestamibi Perfusion Scintigraphy in Patients With Chest Pain and Known or Suspected Coronary Artery Disease

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Abstract

To investigate the prognostic value of dobutamine stress-induced changes in systolic blood pressure (BP) 418 patients (mean age 60 years, 238 men) with chest pain and known or suspected coronary artery disease, who underwent a dobutamine-atropine stress technetium-99m sestamibi myocardial perfusion scintigraphic study, were followed up for 25 ± 15 months. Blood pressure was measured by automatic sphygmomanometry every 3 minutes. A marked decrease and increase in systolic BP from rest to peak were defined as changes of ≥20 mm Hg, and ≥30 mm Hg, respectively. Worst outcome events were cardiac death (n = 30), nonfatal myocardial infarction (n = 17), and hospitalization for congestive heart failure (n = 8). A decrease in systolic BP (prevalence 16%) was associated with older age and higher baseline systolic BP. Fixed and reversible sestamibi perfusion defects and follow-up results were similar to patients without a systolic BP decrease. In contrast, an increase in systolic BP (prevalence 24%) was associated with younger age, lower baseline systolic BP, and with absence of a history of prior congestive heart failure or treatment with angiotensin-converting enzyme inhibitors. Furthermore, these patients had fewer fixed perfusion defects and tended to have fewer annual event rates (3.5% vs 7.5%, p <0.10). In a multivariate model, an increase in systolic BP was not an independent predictor for subsequent events. In conclusion, a dobutamine-induced decrease in systolic BP is not associated with fixed or reversible sestamibi defects or adverse prognosis. An increase in systolic BP, however, is associated with less fixed sestamibi defects and a tendency toward less annual event rates.

During dobutamine-atropine stress technetium-99m sestamibi perfusion imaging in 418 patients, a decrease in systolic blood pressure (BP) ≥20 mm Hg was present in 16% of the patients and an increase in systolic BP ≥30 mm Hg was present in 24% of the patients. A decrease in systolic BP was not associated with fixed and reversible sestamibi perfusion defects or clinical outcome (cardiac death, nonfatal myocardial infarction, congestive heart failure); an increase in systolic BP, however, was associated with less fixed defects and a tendency toward better clinical outcome.

Section snippets

Patient Selection

Over a 4-year period, between November 1990 and October 1994, 418 consecutive patients with chest pain were referred to the nuclear cardiology laboratory at the Thoraxcentre for the evaluation of suspected myocardial ischemia with dobutamine-atropine technetium-99m sestamibi single-photon emission computed tomographic imaging. All patients were unable to perform an adequate exercise test and none had prior heart transplantation, significant congenital or valvular heart disease, unstable angina,

Dobutamine-Induced Decrease in Systolic Blood Pressure

A decrease in systolic BP ≥20 mm Hg was present in 65 patients (16%), and was associated with older age (p <0.001) and higher baseline systolic BP (p <0.0001). Severe, symptomatic hypotension as a test end point was present in only 4 patients (1%). Gender, history of prior myocardial infarction or congestive heart failure, and the use of β blockers, angiotensin-converting enzyme inhibitors or diuretics were not associated with a hypotensive systolic BP response (Table 1Table 2). There were no

Discussion

Generally, dobutamine stress causes an increase in heart rate, a reduction in systemic vascular resistance, a reduction in stroke volume (after an initial increase), and an increase in cardiac output.12, 19, 20Previous dobutamine stress studies have shown that as a net result, in general, there is a mild but significant increase in systolic BP.6, 21This would suggest that, on average, an increase in cardiac output corrects for the decrease in systemic vascular resistance. Although the

Acknowledgements

This study was supported in part by funds from the Dutch Heart Foundation (Grant NHS 94.135), The Hague, The Netherlands, and Cairo University Hospital, Cairo, Egypt.

References (28)

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