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Left ventricular hypertrophy is present in one-half of newly-diagnosed peripheral arterial disease patients
Gary A Wright1, Donald S C Ang, Peter A Stonebridge
1Division of Medicine and Therapeutics, Ninewells Hospital and Medical School, Dundee DD1 9SY, UK.
Insights
Left ventricular hypertrophy (LVH) is highly prevalent in peripheral arterial disease (PAD) patients. Early detection and regression of LVH may reduce cardiac death risk in PAD beyond blood pressure control.
Area of Science:
- Cardiology
- Vascular Medicine
- Cardiovascular Research
Background:
- Peripheral arterial disease (PAD) patients face elevated risks of cardiac death.
- Silent coronary artery disease is a known risk factor, but left ventricular hypertrophy (LVH) may also significantly contribute.
- LVH's role in cardiac mortality among PAD patients warrants further investigation.
Purpose of the Study:
- To determine the prevalence of left ventricular hypertrophy (LVH) at the initial diagnosis of peripheral arterial disease (PAD).
- To assess if LVH contributes significantly to cardiac death risk in PAD patients.
Main Methods:
- Assessed the prevalence of LVH using echocardiography in newly diagnosed PAD patients.
- Indexed left ventricular mass to body surface area for LVH assessment.
- Compared blood pressure measurements (office and 24-h) between patients with and without LVH.
Main Results:
- Echocardiographic LVH was present in 50% of PAD patients at diagnosis.
- Patients with LVH had significantly higher office and 24-h blood pressure readings.
- Standard blood pressure cut-offs partially identified LVH, with 27% of LVH cases below 140/90 mmHg (office) and 24% below 125/80 mmHg (24-h).
Conclusions:
- A high prevalence of LVH exists at the time of PAD diagnosis.
- LVH is common enough in PAD to be a major contributor to cardiac death.
- Future research should explore if screening and regression of LVH reduce cardiac deaths in PAD, independent of blood pressure management.
Objectives:
Peripheral arterial disease (PAD) patients are at high risk of cardiac death. Coincidental but silent coronary disease is obviously a major contributor but left ventricular hypertrophy (LVH) could be a second major contributor.
Methods:
To investigate whether LVH could really be making a large contribution to cardiac death in PAD, we assessed the prevalence of LVH when PAD was first diagnosed.
Results:
The prevalence of echo LVH when left ventricular mass was indexed to body surface area was 50%. Although office blood pressure and 24-h blood pressure were both significantly higher in those with LVH, in clinical practice, a contemporaneous blood pressure measurement (office or 24 h) at the time of PAD diagnosis would only partially identify those with LVH. For example, an office blood pressure cut-off of < 140/90 mmHg was found in 27% of all LVH cases and a 24-h blood pressure cut-off of < 125/80 mmHg was found in 24% of all LVH cases.
Conclusion:
In conclusion, there is already a high prevalence of LVH in patients at first diagnosis of PAD. LVH is therefore common enough in PAD patients to potentially make a major contribution to cardiac death, which means that future research should now investigate whether screening for and regressing LVH when present would actually reduce cardiac deaths over and above merely achieving target blood pressure.
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