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Published on: August 17, 2022
Hypertensive coronary microvascular dysfunction: a subclinical marker of end organ damage and heart failure
Wunan Zhou1,2, Jenifer M Brown3, Navkaranbir S Bajaj4
1Cardiology Branch, Division of Intramural Research, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20814, USA.
Insights
Hypertension increases heart failure risk. Combining myocardial flow reserve (MFR) and global longitudinal strain (GLS) improves risk assessment in hypertensive patients with subclinical dysfunction.
Area of Science:
- Cardiology
- Cardiovascular Imaging
- Hypertension Research
Background:
- Hypertension is a major risk factor for heart failure (HF), often linked to adverse left ventricular (LV) remodeling.
- Subclinical microvascular and myocardial dysfunction are key indicators of early hypertensive heart disease.
Purpose of the Study:
- To assess if myocardial flow reserve (MFR) and global longitudinal strain (GLS) can refine risk stratification for HF in hypertensive patients.
- To investigate the relationship between these markers and LV remodeling patterns.
Main Methods:
- Included 194 hypertensive patients without reduced ejection fraction or significant coronary artery disease.
- Assessed MFR using cardiac positron emission tomography (PET) and GLS via echocardiography.
- Followed patients for a median of 8.75 years for HF hospitalization and composite cardiovascular outcomes.
Main Results:
- Maladaptive LV remodeling was associated with lower MFR and impaired GLS.
- Abnormal MFR and GLS combined significantly increased HF hospitalization risk (adjusted HR 3.21).
- This combined marker predicted higher HF hospitalization risk even in patients with adaptive remodeling (adjusted HR 3.93).
Conclusions:
- Coronary microvascular dysfunction (MFR) and myocardial mechanics (GLS) are associated with subclinical target organ injury in hypertension.
- These markers refine disease characterization and improve HF risk assessment in hypertensive individuals.
- The combination of MFR and GLS offers valuable prognostic information for hypertensive patients at risk of HF.
Aims:
Hypertension is a well-established heart failure (HF) risk factor, especially in the context of adverse left ventricular (LV) remodelling. We aimed to use myocardial flow reserve (MFR) and global longitudinal strain (GLS), markers of subclinical microvascular and myocardial dysfunction, to refine hypertensive HF risk assessment.
Methods And Results:
Consecutive patients undergoing symptom-prompted stress cardiac positron emission tomography (PET)-computed tomography and transthoracic echocardiogram within 90 days without reduced left ventricular ejection fraction (<40%) or flow-limiting coronary artery disease (summed stress score ≥ 3) were included. Global MFR was quantified by PET, and echocardiograms were retrospectively analysed for cardiac structure and function. Patients were followed over a median 8.75 (Q1-3 4.56-10.04) years for HF hospitalization and a composite of death, HF hospitalization, MI, or stroke. Of 194 patients, 155 had adaptive LV remodelling while 39 had maladaptive remodelling, which was associated with lower MFR and impaired GLS. Across the remodelling spectrum, diastolic parameters, GLS, and N-terminal pro-B-type natriuretic peptide were independently associated with MFR. Maladaptive LV remodelling was associated with increased adjusted incidence of HF hospitalization and death. Importantly, the combination of abnormal MFR and GLS was associated with a higher rate of HF hospitalization compared to normal MFR and GLS [adjusted hazard ratio (HR) 3.21, 95% confidence interval (CI) 1.09-9.45, P = 0.034), including in the adaptive remodelling subset (adjusted HR 3.93, 95% CI 1.14-13.56, P = 0.030).
Conclusion:
We have demonstrated important associations between coronary microvascular dysfunction and myocardial mechanics that refine disease characterization and HF risk assessment of patients with hypertension based on subclinical target organ injury.
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Coronary Artery Disease II: Pathophysiology

