Why the study?
Does cessation of long-term antihypertensive therapy lead to redevelopment of hypertension and hemodynamic changes in patients with essential hypertension?
Does cessation of long-term antihypertensive therapy lead to redevelopment of hypertension and hemodynamic changes in patients with essential hypertension?
Cessation of long-term antihypertensive therapy leads to rapid redevelopment of hypertension driven by increases in cardiac index and postural blood pressure responses.
Answers are grounded in this paper and cite their sources.
May indicate rapid BP rebound after antihypertensive cessation; hypothesis-generating for hemodynamic mechanisms in essential hypertension.
We have previously found that the vascular hypertrophy that accounts for the maintenance of a substantial fraction of the elevation of the total peripheral resistance index (TPRI) in essential hypertension can be almost completely reversed by one years antihypertensive treatment (1). On ceasing treatment, blood pressure returns rapidly to pretreatment values suggesting that the original cause of the hypertension is still present. In the present study, 7 patients stopped a standard regimen for 10 weeks after at least 2 years of normotension. In the first week, standing and lying blood pressure increased related to rise in supine cardiac index and TPRI. Thereafter standing pressures, supine systolic blood pressure and cardiac index (CI) increased further, but supine diastolic blood pressure and TPRI did not alter. Changes in measurements of resting sympathetic activity, plasma volume or renin-angiotensin did not account for these observations. The return of hypertension after stopping effective therapy has some features previously described in borderline hypertension, particularly increasing systolic blood pressure, CI and postural blood pressure responses. Some of the changes may reflect the relative preponderance of cardiac and vascular amplifiers.
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Jennings et al. (1984) studied this question.
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