Prevalence and Long-Term Predictors of Left Ventricular Hypertrophy, Late Hypertension, and Hypertensive Response to Exercise After Successful Aortic Coarctation Repair

Abstract

Controversial data exist about the long-term results of aortic coarctation (AC) repair. This study explored the prevalence and predictors of left ventricular (LV) hypertrophy, late hypertension, and hypertensive response to exercise in 48 subjects (age, 15.1 ± 9.7 years) currently followed in the authors' tertiary care hospital after successful AC repair. Data on medical history, clinical examination, rest and exercise echocardiography, and ambulatory blood pressure monitoring were collected. The time from AC repair to follow-up evaluation was 12.9 ± 9.2 years. The prevalence of LV hypertrophy ranged from 23 to 38 %, based on the criteria used to identify LV hypertrophy, and that of concentric geometry was 17 %. One sixth of the patients without residual hypertension experienced late-onset hypertension. One fourth of those who remained normotensive without medication showed a hypertensive response to exercise. Age at AC repair was the strongest independent predictor of LV hypertrophy, defined using indexation either for body surface area (odds ratio [OR], 1.03; p = 0.0090) or for height(2.7) (OR 1.02; p = 0.029), and it was the only predictor of late hypertension (OR 1.06; p = 0.0023) and hypertensive response to exercise (OR 1.09; p = 0.029). The risk of LV hypertrophy was 25 % for repair at the age of 3.4 years but rose to 50 and 75 % for repair at the ages of 5.9 and 8.4 years, respectively. Similar increases were found for the risk of late-onset hypertension and hypertensive response to exercise. A considerable risk of LV hypertrophy, late hypertension, and hypertensive response to exercise exists after successful AC repair. Older age at intervention is the most important predictor of these complications.

Late Coarctation Presenters Suffer Chronic Hypertension Resisting to Medicine Treatment

“…Early-to-midterm outcomes of patients with CoA are excellent, with early mortality rates as low as 2%. However, significant longer-term morbidity remains, particularly with respect to premature systemic HTN (32). This is associated with significant morbidity and early mortality and although early treatment appears to delay its onset, remarkably one third of CoA patients still become HTN by adolescence despite early and effective surgicalrepair [36].…”

“…Early surgery may prevent or delay the onset of HTN. Approximately 30% of patients will be HTN by adolescence despite early surgery and more recent reports observe that about 60% of adults after correction of CoA in childhood are HTN [10,32]. These patients, as mentioned above are at risk of premature CAD, LV systolic as well as diastolic dysfunction, and rupture of aortic or cerebral aneurysms.…”

“…Early studies examining the impact of the renin-angiotensin system on HTN in CoA, concentrated on plasma renin levels with ambiguous results, mostly demonstrating no significant increases in these levels in CoA patients [8]. Subsequent studies have evaluated renin levels following alterations to resting homeostasis, such as fluid depletion or exercise [32]. Although Parker et al [32].…”

“…Subsequent studies have evaluated renin levels following alterations to resting homeostasis, such as fluid depletion or exercise [32]. Although Parker et al [32]. Demonstrated increased pre-operative plasma renin levels following significant volume depletion, the subjects studied were older children (5-16years) and the values were normalized post-operatively including in those who remained HTN, thereby making a causal link for sustained long-term hypertension unlikely.…”

“…Whether this represents early programming is unclear, as this mechanism has not been studied in young pre-operative patients, and adult studies generally recognize endothelial dysfunction therefore rather than a cause of HTN. Diffuse endothelial dysfunction is also likely to affect peripheral vascular resistance, which has the most profound effects on mean and diastolic BP values rather than systolic values and pulse pressure that are commonly raised in HTN CoA patients [8,32]. As highlighted above, we have for the time been, no clear understanding of the pathophysiological pathways that creates HTN in CoA patients, early or late after their successful treatment.…”