ST segment depression elicited by dipyridamole infusion in asymptomatic hypertensive patients.

Lucarini, Alessandra; Lattanzi, Fabio; Marini, Cecilia; Distante, Alessandro; Salvetti, Antonio; LʼAbbate, Antonio

doi:10.1161/01.hyp.16.1.19

Cited by 19 publications

(3 citation statements)

References 28 publications

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“…5 It has been presumed that these ischemic changes are due to subendocardial underperfusion. 6 Our results suggest that such underperfusion could arise from an exaggeration of a redistribution of LV transmural blood flow toward subepicardial muscle layers normally accompanying aortic pressure reduction. Moreover, if this exaggerated redistribution is mainly related to a shift of the lower limit of coronary autoregulation to a higher pressure level, then the persistence of this shift in patients, despite long-term pressure normalization, 39 may also in part explain the paradoxical increase in mortality observed with reduction of arterial diastolic pressure below about 90 mm Hg with antihypertensive therapy.…”

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confidence: 69%

Left ventricular blood flow during aortic pressure reduction in hypertensive dogs.

et al. 1991

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We measured left ventricular blood flow with radioactive microspheres during aortic pressure reduction in 10 open-chest, anesthetized dogs with left ventricular hypertrophy due to chronic hypertension and in 10 matched normotensive dogs. Heart rate and left atrial pressure were held constant, and autonomic reflexes were abolished with ganglionic blockade. Aortic diastolic pressure was lowered from baseline to 90, 75, and 60 mm Hg with an arteriovenous fistula. During aortic pressure reduction, a stepwise decline in the endocardial-to-epicardial flow ratio in hypertrophied hearts from 1.23 ±0.04 at baseline to 0.96±0.09 at a diastolic pressure of 75 mm Hg parallelled that in normal hearts and was not associated with any deterioration in left ventricular performance. However, a further fall in the endocardial-to-epicardial flow ratio to 0.76±0.10 at a diastolic pressure of 60 mm Hg in hypertrophied hearts exceeded that in normal hearts (0.92 ± 0.05, p< 0.05) and was accompanied by evidence of left ventricular isovolumic and end-systolic dysfunction. We conclude that in hearts with pressure-overload left ventricular hypertrophy, aortic pressure reduction causes a transmural blood flow redistribution from subendocardial to subepicardial muscle layers. At moderately low aortic pressures, this redistribution is more pronounced than in normal hearts and is associated with functional evidence of myocardial ischemia. {Hypertension 1991;18:665-673) S everal lines of evidence suggest that lowering aortic blood pressure in the setting of chronic hypertension may have deleterious effects on the heart. Experimental studies have demonstrated that in hearts with hypertension-induced left ventricular (LV) hypertrophy, LV isovolumic indexes 1 and pump function 2 -3 are impaired at reduced aortic pressure levels that are well-tolerated by normal hearts. These findings are in accord with clinical studies that have noted either asymptomatic electrocardiographic changes 4 -6 or overt symptoms of myocardial ischemia 7 after acute pressure reduction in hypertensive patients. Moreover, epidemiological studies that have described a U-shaped 8 or J-shaped relation 9 between the level of blood pressure after treatment and the incidence of cardiac mortality have led to the suggestion that excessive reduction of blood pressure with antihypertensive therapy might precipitate myocardial ischemia and infarction. 10Since animal studies using electrical pacing 11 and coronary artery constriction 12 have shown that the hypertrophied left ventricle is susceptible to subendocardial perfusion deficits, one possible explanation for any detrimental effects of aortic pressure reduction in hypertrophied hearts is an alteration in LV transmural blood flow patterns. We have previously shown that in normal hearts, moderate aortic pressure reduction redistributes LV blood flow from subendocardial to subepicardial muscle layers, without depression of LV isovolumic indexes or electrical evidence of myocardial ischemia.13 It is not known, however, if aortic pre...

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confidence: 69%

Left ventricular blood flow during aortic pressure reduction in hypertensive dogs.

et al. 1991

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“…In the present study, out of 8 patients with normal perfusion on SPECT, 2 were women, in both of whom coronary angiogram was not performed, but they had no cardiac event for 24 months after the study. It is also reported that hypertensive patients frequently have ST-segment depression during myocardial SPECT with adenosine loading [22]. If hypertension is present for decades, coronary blood flow and resistance increase and the coronary flow reserve decreases [25].…”

Section: Discussionmentioning

confidence: 98%

“…In contrast to the above observations, severe myocardial ischemia, known as ''balanced ischemia,'' was also reported to occur in patients with ST-segment depression and normal myocardial perfusion on SPECT [20,21]. Some reports, on the contrary, state that ST-depression during pharmacological stress with normal perfusion SPECT implies a good prognosis particularly in women and hypertensive patients [21,22]. According to the previous study, the prevalence of ST-segment depression during adenosine loading in women was higher than that in men [21].…”

Section: Discussionmentioning

confidence: 99%