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Parallel increase in carotid, brachial and left ventricular cross-sectional areas in arterial hypertension
F Fantini1, G Barletta, R Del Bene
1Cardiology and Internal Medicine, University of Florence, Italy.
Insights
Arterial hypertension causes arterial enlargement and left ventricular (LV) hypertrophy. These changes in vessel and heart geometry are proportionally linked, suggesting a common underlying mechanism in untreated hypertensive patients.
Area of Science:
- Cardiovascular Physiology
- Vascular Biology
- Clinical Hypertension Research
Background:
- Limited data exist on the relationship between vascular geometry and left ventricular (LV) hypertrophy in arterial hypertension.
- Understanding these geometric changes is crucial for managing hypertensive cardiovascular complications.
Purpose of the Study:
- To investigate arterial and LV geometry alterations in untreated patients with mild-to-moderate arterial hypertension.
- To explore the correlation between vascular and myocardial geometric changes.
Main Methods:
- Cross-sectional study involving 95 untreated hypertensive patients and 23 healthy controls.
- Measurements included left ventricular dimensions, carotid and brachial artery diameter, and intimal-medial thickness (IMT).
- Calculation of arterial and myocardial wall cross-sectional areas (CSAs); LV hypertrophy defined by established criteria.
Main Results:
- Hypertensive patients with LV hypertrophy exhibited arterial enlargement (increased CSAs) in carotid and brachial arteries.
- The left ventricle developed concentric hypertrophy.
- Both arterial and LV CSAs correlated directly with systolic blood pressure (BP), with improved correlation after BP correction.
Conclusions:
- Untreated mild-to-moderate arterial hypertension leads to proportional enlargement of carotid and brachial arteries and the development of LV hypertrophy.
- These findings suggest a common pathway modulating the geometric effects of hypertension on peripheral arteries and the left ventricle.
Abstract:
Few data have been published about the relation between the vessels geometry and development of left ventricular (LV) hypertrophy in patients with arterial hypertension. The aim of this study is to describe arterial and LV geometry changes due to mild-to-moderate arterial hypertension in an untreated hypertensive population. In 95 untreated patients with mild-to-moderate hypertension and 23 age- and sex-matched healthy normotensives, we measured the end-diastolic diameter and wall thickness of the left ventricle and the internal diameter and intimal-medial thickness (IMT) of carotid and brachial arteries. From these data, the cross-sectional areas (CSAs) of arterial and myocardial walls were calculated. Hypertensive patients were further subdivided on the basis of the presence of LV hypertrophy defined according to Devereux et al as anatomical LV mass >125 g/m. In hypertensive patients with hypertrophy, carotid and brachial CSAs increased, without significant changes in thickness/diameter ratio (arterial 'enlargement'), while the left ventricle developed 'concentric' hypertrophy. Arterial and LV CSAs showed a significant direct correlation with systolic blood pressure (BP). However, when data were corrected for BP, the correlation between the increase in arterial and LV CSAs became much improved than for the raw data. In conclusion patients with untreated mild-to-moderate hypertension, both carotid and brachial arterial walls showed an enlargement that was proportional to the development of LV hypertrophy. These results suggest that the effects of arterial hypertension on carotid, brachial and LV wall geometry have a common modulation.
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