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Differential Response in Left Ventricular Mass and Arterial Resistive Index following Fosinopril Therapy

F Veglio1, L Gastaldi, M Frascisco

  • 1Department of Medicine and Experimental Oncology, University of Turin, Turin, Italy.

Insights

Long-term ACE inhibitor therapy significantly reduced blood pressure and left ventricular mass in hypertensive patients. However, arterial stiffness changes varied across different vessels, with common carotid and renal hilum arteries showing improvement.

Area of Science:

  • Cardiology
  • Hypertension Research
  • Pharmacology

Background:

  • Essential hypertension is a leading cause of cardiovascular disease.
  • Left ventricular hypertrophy and arterial stiffness are key indicators of cardiovascular risk.
  • Angiotensin-converting enzyme (ACE) inhibitors are a cornerstone in hypertension management.

Purpose of the Study:

  • To evaluate the effects of 1-year ACE inhibitor (fosinopril) therapy on left ventricular mass and arterial stiffness in patients with mild to moderate essential hypertension.
  • To assess the differential impact of treatment on resistive index (RI) in renal and carotid arteries.

Main Methods:

  • Twenty-six patients with essential hypertension received either placebo or 20 mg/day fosinopril for 12 months.
  • Measurements included 24-hour ambulatory blood pressure monitoring, echocardiography for left ventricular mass, and echo-Doppler for carotid and renal artery resistive indices.
  • Resistive index (RI) was used to quantify arterial impedance.

Main Results:

  • Fosinopril treatment significantly reduced 24-hour blood pressure (BP), left ventricular mass, and RI in common carotid and hilum renal arteries.
  • No significant reduction was observed in interlobar renal RI or internal carotid artery RI.
  • A strong correlation was found between BP reduction and left ventricular mass changes, but not with arterial RI parameters.

Conclusions:

  • Long-term fosinopril treatment effectively reduces BP and left ventricular mass in hypertensive patients.
  • The therapy induces differential changes in arterial stiffness, improving impedance in proximal vessels but not distal intrarenal or internal carotid arteries.
  • Arterial impedance modifications in the common carotid and renal hilum arteries were largely independent of the observed 24-hour BP reduction.

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