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Left Ventricular Hypertrophy Predicts Cardiovascular Events in Hypertensive Patients With Coronary Artery
Chagai Grossman1,2, Michael Levin2,3, Nira Koren-Morag2,4
1Department of Internal Medicine F and the Rheumatology unit, The Chaim Sheba Medical Center, Tel-Hashomer, Israel.
Insights
Left ventricular hypertrophy (LVH) significantly increases cardiovascular risk, but only when coronary artery calcification (CAC) is also present. This highlights the combined impact of LVH and CAC on cardiovascular events in hypertensive patients.
Area of Science:
- Cardiology
- Hypertension Research
- Diagnostic Imaging
Background:
- Coronary artery calcification (CAC) is a known indicator of increased cardiovascular (CV) risk.
- Left ventricular hypertrophy (LVH) independently predicts CV events.
- The interplay between CAC and LVH in determining CV risk requires further elucidation.
Purpose of the Study:
- To evaluate the combined impact of LVH and CAC on cardiovascular risk in asymptomatic hypertensive patients.
- To determine if LVH poses a significant CV risk in the presence or absence of CAC.
Main Methods:
- Analysis of asymptomatic hypertensive patients from the INSIGHT trial.
- Baseline assessment of LVH via echocardiography and CAC via computed tomography.
- Long-term follow-up for the primary endpoint of the first CV event.
Main Results:
- Patients with both LVH and CAC exhibited a significantly higher rate of CV events compared to those with only one or neither condition.
- LVH alone did not significantly increase CV event rates in the absence of CAC.
- LVH presence nearly doubled the CV event rate in patients with CAC (61.4% vs. 36.5%).
Conclusions:
- Both LVH and CAC are independent predictors of CV events in asymptomatic hypertensive individuals.
- The heightened CV risk associated with LVH is predominantly observed in the presence of concurrent CAC.
Background:
Coronary artery calcification (CAC) is associated with increased cardiovascular (CV) risk. Left ventricular hypertrophy (LVH) is an independent risk factor for CV events. Our aim was to estimate the relative CV risk of LVH in the presence of CAC.
Methods:
We included asymptomatic hypertensive patients who were enrolled in the calcification arm of the INSIGHT (International Nifedipine Study Intervention as Goal for Hypertension Therapy). Patients had baseline echocardiography and computed tomography to assess CAC. The primary end-point was the first CV event.
Results:
Two hundred and fifty-two subjects (mean age 64.7 ± 5.5 years, 54% men) were followed for a mean of 13.3 ± 2.6 years. 72 patients (28.5%) had LVH and 159 patients (63%) had CAC. During follow up, 89 patients had a first CV event. The rate of CV events was higher in those with than in those without CAC (43.4% vs. 21.5%, P < 0.01) and in those with than in those without LVH (44% vs. 31.6%, P < 0.01). However, LVH had no effect on CV events in the absence of CAC, whereas LVH almost doubled the rate of CV events (61.4% vs. 36.5%, P < 0.01) in the presence of CAC. In comparison to patients without CAC and without LVH the hazard ratio for CV event in those with LVH was 1.46 (95% confidence interval [CI], 0.50-4.21) in those without CAC and 4.4 (95% CI, 2.02-9.56) in those with CAC.
Conclusions:
LVH and CAC independently predict CV events in asymptomatic hypertensive patients. However, the risk of LVH is mainly observed in those with CAC.