TY - JOUR
T1 - Hypertensive coronary microvascular dysfunction
T2 - A subclinical marker of end organ damage and heart failure
AU - Zhou, Wunan
AU - Brown, Jenifer M.
AU - Bajaj, Navkaranbir S.
AU - Chandra, Alvin
AU - Divakaran, Sanjay
AU - Weber, Brittany
AU - Bibbo, Courtney F.
AU - Hainer, Jon
AU - Taqueti, Viviany R.
AU - Dorbala, Sharmila
AU - Blankstein, Ron
AU - Adler, Dale
AU - O'Gara, Patrick
AU - Di Carli, Marcelo F.
N1 - Funding Information:
National Institutes of Health (5T32HL094301 to W.Z., A.C., S.D., and BW), (T32HL007604 to J.M.B.), (K23HL135438 to V.R.T.), and (R01HL132021 toM.D.C.).
Funding Information:
fees from Pfizer and Proclara. R.B. reports grants from Amgen and Astellas. M.F.D.C. reports grants from Gilead Sciences and Spectrum Dynamics and consulting honoraria from Bayer and Janssen. P.O. reports support from Medtrace. The other authors declared that they have no relevant relationships to disclose.
Publisher Copyright:
© 2020 Published on behalf of the European Society of Cardiology. All rights reserved.
PY - 2020/7/1
Y1 - 2020/7/1
N2 - 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.
AB - 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.
KW - Coronary microvascular dysfunction
KW - Heart failure
KW - Hypertension
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U2 - 10.1093/eurheartj/ehaa191
DO - 10.1093/eurheartj/ehaa191
M3 - Article
C2 - 32221588
AN - SCOPUS:85087304519
SN - 0195-668X
VL - 41
SP - 2366
EP - 2375
JO - European heart journal
JF - European heart journal
IS - 25
ER -