Alexander P Taylor1, Rosario V Freeman2, Matthew A Bartek3, Sherene Shalhub4. 1. Department of Internal Medicine, University of Washington, Seattle, Wash. 2. Division of Cardiology, Department of Internal Medicine, University of Washington, Seattle, Wash. 3. Department of Surgery, University of Washington, Seattle, Wash. 4. Division of Vascular Surgery, Department of Surgery, University of Washington, Seattle, Wash. Electronic address: shalhub@uw.edu.
Abstract
OBJECTIVE: Data regarding the cardiac abnormalities associated with Stanford type B aortic dissection (TBAD) and whether these abnormalities are related to outcomes are limited. We describe the prevalence of cardiac abnormalities in patients with TBAD as detected by echocardiography. METHODS: This retrospective review included patients with TBAD presenting between 1990 and 2016. Echocardiograms performed within 6 weeks of acute TBAD were reviewed. Cardiac function, valve abnormalities, and stigmata of hypertensive heart disease including left ventricular hypertrophy (LVH) were ascertained. Characteristics of patients who did and did not receive echocardiograms were compared. Outcomes of patients with and without evidence of LVH on echocardiography were also compared. RESULTS: Of 239 patients with TBAD, 90 had echocardiograms performed within 6 weeks of acute TBAD (74% male; mean age, 57.8 ± 13.2 years). Echocardiograms were obtained at a median of 2 days (range, 0-41 days) from acute TBAD. Patients who had echocardiograms were more likely to present with malperfusion (28% vs 14%; P < .01) and had a trend toward increased operative repair during the subacute phase (17.4% vs 9.5%; P = .07) compared with patients who did not receive an echocardiogram. A majority of patients (57%) had at least mild LVH, including 39% of patients without a prior diagnosis of hypertension. Fibrocalcific changes associated with hypertension, including aortic sclerosis and mitral annular calcification, were noted in 40% and 11% of the patients, respectively. Among patients with LVH, there was a trend toward higher all-cause mortality (35% vs 23%; P = .21) and a younger age at death (58 ± 14 years vs 66 ± 13 years; P = .19) despite a similar age at TBAD onset. In a multivariable analysis controlling for age, sex, and admission estimated glomerular filtration rate, LVH independently predicted all-cause mortality (hazard ratio, 2.38; 95% confidence interval, 1.02-5.56; P = .04). CONCLUSIONS: LVH and other findings of hypertensive heart disease are common in patients with TBAD. LVH predicted all-cause mortality after TBAD in this small group of patients. Further exploration of the relationship between the chronic effects of hypertension and using LVH as an objective biomarker to risk stratify patients with TBAD and long-term outcomes after TBAD is warranted.
OBJECTIVE: Data regarding the cardiac abnormalities associated with Stanford type B aortic dissection (TBAD) and whether these abnormalities are related to outcomes are limited. We describe the prevalence of cardiac abnormalities in patients with TBAD as detected by echocardiography. METHODS: This retrospective review included patients with TBAD presenting between 1990 and 2016. Echocardiograms performed within 6 weeks of acute TBAD were reviewed. Cardiac function, valve abnormalities, and stigmata of hypertensive heart disease including left ventricular hypertrophy (LVH) were ascertained. Characteristics of patients who did and did not receive echocardiograms were compared. Outcomes of patients with and without evidence of LVH on echocardiography were also compared. RESULTS: Of 239 patients with TBAD, 90 had echocardiograms performed within 6 weeks of acute TBAD (74% male; mean age, 57.8 ± 13.2 years). Echocardiograms were obtained at a median of 2 days (range, 0-41 days) from acute TBAD. Patients who had echocardiograms were more likely to present with malperfusion (28% vs 14%; P < .01) and had a trend toward increased operative repair during the subacute phase (17.4% vs 9.5%; P = .07) compared with patients who did not receive an echocardiogram. A majority of patients (57%) had at least mild LVH, including 39% of patients without a prior diagnosis of hypertension. Fibrocalcific changes associated with hypertension, including aortic sclerosis and mitral annular calcification, were noted in 40% and 11% of the patients, respectively. Among patients with LVH, there was a trend toward higher all-cause mortality (35% vs 23%; P = .21) and a younger age at death (58 ± 14 years vs 66 ± 13 years; P = .19) despite a similar age at TBAD onset. In a multivariable analysis controlling for age, sex, and admission estimated glomerular filtration rate, LVH independently predicted all-cause mortality (hazard ratio, 2.38; 95% confidence interval, 1.02-5.56; P = .04). CONCLUSIONS: LVH and other findings of hypertensive heart disease are common in patients with TBAD. LVH predicted all-cause mortality after TBAD in this small group of patients. Further exploration of the relationship between the chronic effects of hypertension and using LVH as an objective biomarker to risk stratify patients with TBAD and long-term outcomes after TBAD is warranted.
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