Background Early detection of risk factors for left ventricular (LV) dysfunction may be useful in patients with high blood pressure (HBP). Methods Patient from an outpatient HBP clinic underwent a two-dimensional Doppler-coupled echocardiography with determination of LV global longitudinal strain (GLS) by speckle-tracking. Results Among 200 patients (mean age 61.7 ± 9.7 years), 155 were overweight, 93 had diabetes, 83 had dyslipidemia, and 109 had uncontrolled HBP. LV hypertrophy (LVH) was found in 136 patients (68%), including concentric ( n = 106) and eccentric ( n = 30) LVH. Diastolic dysfunction patterns were observed in 178 patients (89%), and increased filling pressures were observed in 37 patients (18.5%). GLS ranged from -25% to -11.6% (mean -16.9 ± 3.2%). Low GLS values (>-17%) were found in 91 patients (45.5%), 68 with and 23 without LVH. In univariate analysis, a reduced GLS was associated with HBP lasting for >10 years (odds ratio (OR) = 3.51, 95% confidence interval (CI) 1.73-7.09; p = 0.002), uncontrolled HBP (OR = 3.55, 95% CI 1.96-6.43; p < 0.0001), overweight (OR = 2.01, 95% CI 0.93-4.31; p = 0.0028), diabetes (OR = 2.21, 95% CI 1.25-3.90; p = 0.006), dyslipidemia (OR = 2.16, 95% CI 1.22-3.84; p = 0.008), renal failure (OR = 4.27, 95% CI 1.80-10.10; p = 0.001), an increased Cornell index (OR = 3.70, 95% CI 1.98-6.90; p < 0.0001), concentric LVH (OR = 9.26, 95% CI 2.62-32.73; p = 0.001), remodeling (OR = 8.51, 95% CI 2.18-33.23; p = 0.002), and filling pressures (OR = 7.1, 95% CI 2.9-17.3; p < 0.0001). In multivariable analysis, duration of HBP ( p = 0.038), uncontrolled BP ( p = 0.006), diabetes ( p = 0.023), LVH ( p = 0.001), and increased filling pressures ( p = 0.003) remained associated with GLS decline. Conclusion Early impairment of LV function, detected by a reduced GLS, is associated with long-lasting, uncontrolled HBP, overweight, related metabolic changes, and is more pronounced in patients with LVH.

Background: Although the combination of high blood pressure (HBP) and type 2 diabetes (T2DM) increases the risk of left ventricular (LV) dysfunction, the impact of T2DM on LV geometry and subclinical dysfunction in hypertensive patients and normal ejection fraction (EF) has been infrequently evaluated. Methods: Hypertensive patients with or without T2DM underwent cardiac echocardiography coupled with LV global longitudinal strain (GLS) assessment. Results: Among 200 patients with HBP (mean age 61.7 ± 9.7 years) and EF > 55%, 93 had associated T2DM. Patients with T2DM had a higher body mass index (29.9 ± 5.1 kg/m2 vs. 29.3 ± 4.7 kg/m2, p = 0.025), higher BP levels (158 ± 23/95 ± 13 vs. 142 ± 33/87 ± 12 mmHg, p = 0.003), a higher LV mass index (115.8 ± 32.4 vs. 112.0 ± 24.7 g/m2, p = 0.004), and higher relative wall thickness (0.51 ± 0.16 vs. 0.46 ± 0.12, p = 0.0001). They had more frequently concentric remodeling (20.4% vs. 16.8%, p < 0.001), concentric hypertrophy (53.7% vs. 48.6%, p < 0.001), elevated filling pressures (25.8 vs. 12.1%, p = 0.0001), indexed left atrial volumes greater than 28 mL/m2 (17.2 vs. 11.2%, p = 0.001), and a reduced GLS less than −18% (74.2 vs. 47.7%, p < 0.0001). After adjustment for BP and BMI, T2DM remains an independent determinant factor for GLS decline (OR = 2.26, 95% CI 1.11–4.61, p = 0.023). Conclusions: Left ventricular geometry and subclinical LV function as assessed with GLS are more impaired in hypertensive patients with than without T2DM. Preventive approaches to control BMI and risk of T2DM in hypertensive patients should be emphasized.

Background: The assessment of the longitudinal component of left ventricular (LV) function is of major clinical importance for the early detection of LV contractile impairment. The aim of this study was to determine the impact of uncontrolled hypertension, on LV longitudinal systolic performance. Methods: The study population included 400 hypertensive patients: 271 patients with uncontrolled blood pressure (BP) and 112 without controlled BP, all patients underwent a complete ultrasound evaluation with calculation of the LV mass, evaluation of diastolic function as well as longitudinal systolic function. Results: Conventional echo demonstrated that uncontrolled patients had increased LV mass (P 0.007), LA (left auricular) dimension (P 0.004), left ventricular wall thickness and impairment of diastolic function (E/E’6 ± 2.1 vs 7.4 ±3.0 P=0.001) while no affection of systolic function could be detected. By deformation imaging, there was a reduction in longitudinal strain (apical 4 view -16.2 ±2.9 vs -18.2± 2.6 P 0.02, apical 3 view -17.3 ± 3.3 vs. -18.9 ± 4.1 P 0.01). Similarly systolic strain rate (SRsys) and early diastolic SR (SRe) reduced significantly in longitudinal direction. Conclusion: Although EF was not different between uncontrolled patients and controls, LV longitudinal strain and strain rate by 2D speckle tracking were lower in the uncontrolled group.

La double discordance est une cardiopathie congénitale complexe extrêmement rare, elle se caractérise par une discordance auriculo-ventriculaire suivie d’une autre discordance ventriculo-artérielle. Son diagnostic est posé généralement à l’âge adulte par des examens d’imagerie. Son pronostic dépend essentiellement des autres malformations congénitales cardiaques associées, des arythmies et des troubles de la conduction, ainsi que de la fonction systolique du ventricule droit en position systémique. Nous rapportons le cas d’un patient âgé de 23 ans, porteur d’une cardiopathie congénitale complexe cyanogène. Il s’agit d’une double discordance associée à une large communication interventriculaire sous aortique avec un shunt inversé et une hypoplasie de l’artère pulmonaire. Ce diagnostic a été confirmé par l’imagerie multimodale. Non opéré, le patient a vu son stade fonctionnel s’aggraver rapidement avec une dyspnée qui est passée d’un stade I à un stade III-IV de la New York Heart Association (NYHA), et apparition de signes hypoxiques et congestifs. A travers cette observation, nous avons précisé les caractéristiques anatomocliniques de cette cardiopathie congénitale complexe cyanogène, son exploration, ses options thérapeutiques, ainsi que le rôle péjoratif de son association avec d’autres malformations congénitales.