OBJECTIVE: To evaluate the effects of aliskiren on blood pressure and myocardial functionassessed by global longitudinal strain in patients with uncontrolled arterial hypertension.
PATIENTS AND METHODS: Forty-fi ve patients were included in the study (29 males, 16 females,mean age 58.7 ± 12.4 years) with BP > 140/90 mmHg despite treatment with combined antihypertensivetherapy and echocardiographic data for diastolic dysfunction: Е/Е’ratio ≤8, Е/А ratio < 0.8, deceleration time (DT) > 200 msec. Aliskiren (2 х 150 mg per day) wasadded to the previous therapy. The follow-up period was 1 year, including monthly clinicalvisits. Echocardiographic assessment of the left ventricular function by longitudinal strainand Doppler analysis of the trans-mitral blood flow was performed at months 1, 6, 12.
RESULTS: The baseline systolic and diastolic blood pressures scores were 153.4 ± 14.4/99.2± 6.7 mmHg and 157.6 ± 12.5/97.3 ± 8.2 mmHg for males and females, respectively. Thesystolic and diastolic values at 1 month were 131.7 ± 7.4/83.6 ± 5.2 mmHg for males and132.4 ± 5.3/81.8 ± 6.9 mmHg for females (р < 0.05 vs. baseline). The baseline Е/Е’ was 6.5± 0.9, Е/А - 0.6 ± 001, DT - 258 ± 32.7 msec. These indicators at month 12 were as follows:Е/Е’ - 7.0 ± 0.64, Е/А - 0.7 ± 0.05, DT - 239 ± 16.5 msec, р = NS. Baseline global longitudinalstrain in males was -10.4 ± 0.7% and -11.0 ± 0.9% in females and at month 12 - 16.3 ± 0.9%and -17.5 ± 0.7% for males and females, respectively, р < 0.05. For the period of follow-upno adverse effects due to aliskiren treatment were registered.
CONCLUSIONS: Adding aliskiren to combined antihypertensive therapy leads to significantimprovement of hypertension control and myocardial function assessed by global longitudinalstrain.
Introduction: The clinical significance of inflammation (and markers such as resistin, hsCRP) and oxidative stress (e.g. 8-isoprostanes) for microvascular disease (MVD) and coronary artery disease (CAD) is still elusive.
Aims: To determine the role of the markers for inflammation and oxidative stress as independent markers for MVD.
Methods: Ninety consecutive patients were recruited: twenty-five of them had CAD; thirty – MVD and thirty-five were controls. The latter included patients with atypical chest pain, risk factors, lack of coronary artery disease and negative adenosine test. Coronary angiography was performed in all participants. The adenosine test was performed in those without CAD, hs CRP, resistin in plasma and urine 8-isoprostanes were measured. The correlation of all these indicators with CAD and MVD was analyzed.
Results: The 8-isoprostanes showed significant differences between patients with MVD and CAD (0,055/0,52 pg/mmol Cre; p = 0,028). The same trend was found between CAD patients and the control group (0,055/0,003 pg/mmol Cre; p = 0,041); as well as between those with MVD and the control group (0,52/0,003 pg/mmol Cre; p = 0,001). The highest values of 8-isoprostanes were detected in patients with MVD – 0,52 pg/mmol Cre. Markers for inflammation were similar in patients with MVD and CAD (hsCRP- p = 0,091; resistin − p = 0,32).
Conclusions: hs CRP, resistin and 8-isoprostanes are involved in the pathogenesis of both CAD and MVD. However, oxidative stress is probably more important for MVD, therefore 8-isoprostanes can be a part of panel of markers for its detection and analysis.