Zaporožskij Medicinskij Žurnal (Dec 2013)
Structural and functional changes in the heart and clinical features of heart failure with preserved left ventricular ejection fraction in patients after myocardial infarction, comorbided with arterial hypertension
Abstract
Recently, much attention was paid to left ventricular diastolic dysfunction and its role in the occurrence of chronic heart failure. In patients after myocardial infarction, diastolic dysfunction often precedes systolic dysfunction and predicts prognosis. In patients after myocardial infarction, diastolic dysfunction is caused by a violation of early diastolic relaxation in the area of increasing stiffness. Diastolic dysfunction is formed by hypertrophy, fibrosis, myocardial ischemia and arterial hypertension. Given the important role of diastolic dysfunction in the formation of heart failure in postinfarction patients with concomitant arterial hypertension, the mechanisms of its impact on clinical features and structural-functional changes of the heart is an actual problem. Objective: To determine the structural and functional changes in the heart and clinical features of heart failure with preserved left ventricular ejection fraction in patients after myocardial infarction with concomitant arterial hypertension. Materials and methods: In 91 patients with post-infarction cardiosclerosis and preserved left ventricular ejection fraction (EF > 45 %) with arterial hypertension were investigated structural and functional changes in the heart and clinical features of heart failure by assessing clinical status and ultrasound of the heart. Prescription myocardial infarction ranged from 2 months to 3 years. Patients were divided into 3 groups. The first group included 50 patients with diastolic dysfunction and symptoms of heart failure (mean age 64,1 ± 1,2 years). In the second group were 31 patients with diastolic dysfunction without heart failure symptoms (mean age 59,5 ± 1,6 years). The third group consisted of 10 patients without diastolic dysfunction and manifestations of heart failure (mean age 57 ± 2,8 years). Results and discussion: 10% patients with postinfarction cardiosclerosis and concomitant hypertension with diastolic heart failure had NYHA class I, 32% - NYHA class II, 48% - NYHA class III and 10% have NYHA class IV. In the first group revealed a significant increase of left ventricular end diastolic volume (13,8%, p <0,05), left ventricular end systolic volume (14,9%, p <0,05) and left atrial volume index (35%, p <0,05) compared with patients from the second group. Patients from the second group had a significant increase of left ventricular mass index (15,2%, p <0,05), left ventricular posterior wall ( 12,8%, p <0,05) and interventricular septum (10%, p <0,05) compared with patients from the third group. Patients from the first group had a higher E/E ' ratio (26%, p <0,05) compared with patients from the second group. In patients from the second group revealed decreased E/A (30,8%, p <0,05), E '(35,7%, p <0,05) and increased E/E' (13, 3%, p <0,05) compared with patients from the third group. Patients after myocardial infarction with arterial hypertension and diastolic heart failure had diastolic dysfunction mainly on the type of violation of relaxation (74%). 22% of these patients had pseudonormal type of diastolic dysfunction and 4% had restrictive LV filling type. Conclusion: In patients with post-infarction cardiosclerosis and diastolic heart failure with arterial hypertension severity of clinical manifestations of heart failure correlates with left atrial volume index and markers of diastolic dysfunction such as E' and E/E'. In patients with post-infarction cardiosclerosis and arterial hypertension with diastolic heart failure had predominantly concentric hypertrophy with increased left atrial volume index and moderate left ventricular dilatation and mild diastolic dysfunction. In patients after myocardial infarction with arterial hypertension and asymptomatic diastolic dysfunction observed structural and functional changes in the type of concentric hypertrophy with thickened walls and increased left ventricular mass index.
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