Key result
Captopril regresses LVH and abolishes cardiocyte vulnerability to acute hypoxia better than hydralazine.
Why the study?
Left ventricular hypertrophy secondary to pressure overload leads to perfusion abnormalities that may cause cardiocyte intracellular damage during acute hypoxia, and it is unclear if regression of LVH reduces this vulnerability.
Does regression of left ventricular hypertrophy with antihypertensive therapy prevent cardiocyte damage from acute hypoxia in hypertensive rats?
Population
Six-month-old spontaneously hypertensive and normotensive Wistar-Kyoto rats
Comparison
Captopril or hydralazine with hydrochlorothiazide treatment vs control
Design
Preclinical experimental study with acute hypoxic stress
Follow-up
3 months
Authors
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LVH regression may protect against hypoxic damage beyond BP reduction in rat models; leaves open translation to human hypertension therapy.
Does regression of left ventricular hypertrophy with antihypertensive therapy prevent cardiocyte damage from acute hypoxia in hypertensive rats?
Regression of left ventricular hypertrophy, rather than blood pressure reduction alone, is necessary to protect cardiocytes from acute hypoxic damage in hypertensive models.
Canby et al. (1990) studied Left ventricular hypertrophy and hypertension. Captopril or hydralazine with hydrochlorothiazide vs. Control was evaluated on Morphologic evidence of hypoxic damage. Captopril treatment induced regression of left ventricular hypertrophy and abolished cardiocyte vulnerability to acute hypoxic damage, whereas hydralazine only caused a small reduction.
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