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The effects on cardiac arrhythmias of antihypertensive therapy causing regression of left ventricular hypertrophy
1The Peart-Rose Clinic, Department of Cardiology, St. Mary's Hospital, London, England.
Insights
Antihypertensive therapy effectively reduced left ventricular hypertrophy (LVH) and ventricular ectopics initially. However, the reduction in ventricular ectopics was not sustained long-term despite continued treatment.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Hypertension is a significant risk factor for left ventricular hypertrophy (LVH).
- LVH is associated with an increased risk of cardiac arrhythmias.
- Antihypertensive therapies aim to reduce cardiovascular risk by controlling blood pressure and mitigating LVH.
Purpose of the Study:
- To investigate the impact of antihypertensive therapy on left ventricular hypertrophy (LVH) regression.
- To assess the effects of this therapy on cardiac arrhythmias, specifically ventricular and supraventricular ectopics.
Main Methods:
- 26 hypertensive subjects received ramipril, with felodipine added if necessary.
- Blood pressure and left ventricular mass index (LVMI) were monitored for 6 months post-control.
- Cardiac arrhythmias were assessed by counting ventricular and supraventricular ectopics.
Main Results:
- Antihypertensive therapy significantly reduced LVMI, indicating LVH regression.
- Systolic blood pressure reduction correlated with LVMI decrease.
- Ventricular ectopics initially decreased but were not sustained.
- Supraventricular ectopics decreased after 6 months of treatment, but not significantly.
Conclusions:
- Ramipril and felodipine therapy effectively regressed left ventricular hypertrophy.
- The therapy did not result in a sustained reduction of ventricular ectopic activity.
- Further research is needed to understand long-term arrhythmia management in hypertensive patients with LVH.
Abstract:
To examine the effects of antihypertensive therapy causing regression of left ventricular hypertrophy on cardiac arrhythmias, 26 hypertensive subjects were treated with ramipril with felodipine if required, and followed for 6 months after blood pressure control. Compared with baseline, left ventricular mass index (LVMI) was significantly reduced both at blood pressure control and after a further 6 months of treatment (baseline, blood pressure control, 6 months after blood pressure control; LVMI 142 +/- 3.6, 131 +/- 3.4, 123 +/- 3.8* g/m2, *P < .01 compared with baseline). There was a significant relationship between the decrease in systolic blood pressure and the decrease in LVMI after 6 months of blood pressure control compared with baseline (r = 0.41, P = .05). Compared with baseline, the average total number of ventricular ectopics decreased after blood pressure was controlled (88 +/- 59 and 21 +/- 12 respectively); however this reduction was not maintained after 6 months of further treatment, either before (78 +/- 50) or after drug washout (86 +/- 40). Compared with baseline (639 +/- 590) supraventricular ectopic total was not initially reduced after blood pressure control (650 +/- 604), but was reduced after a further 6 months of treatment (294 +/- 261). This reduction was maintained after drug washout (267 +/- 254), although this did not reach statistical significance. Radionuclide scanning at baseline was not a predictor of patients with the highest risk of arrhythmia and there was no correlation between improvement or worsening of a defect with changes in ventricular ectopic total. In conclusion, antihypertensive therapy with ramipril and felodipine, although causing regression of left ventricular hypertrophy did not lead to a sustained reduction in ventricular ectopic total.