Структурно-функциональное ремоделирование миокарда левого желудочка у больных со стабильной стенокардией и артериальной гипертензией в зависимости от выраженности гипертрофии левого желудочка
Структурно-функциональное ремоделирование миокарда левого желудочка у больных со стабильной стенокардией и артериальной гипертензией в зависимости от выраженности гипертрофии левого желудочка
Структурно-функциональное ремоделирование миокарда левого желудочка у больных со стабильной стенокардией и артериальной гипертензией в зависимости от выраженности гипертрофии левого желудочка
Цель исследования: изучить параметры структурно-функционального состояния миокарда левого желудочка (ЛЖ) у больных со стабильной стенокардией II–III функционального класса в сочетании с артериальной гипертензией (АГ) в зависимости от выраженности гипертрофии левого желудочка (ГЛЖ). Материал и методы: обследованы 90 больных со стабильной стенокардией в сочетании с АГ и ГЛЖ. Оценивали взаимосвязь выраженности ГЛЖ с показателями систолической и диастолической функции ЛЖ, уровнями сывороточных маркеров коллагенолиза миокарда и NT-концевого фрагмента мозгового натрийуретического пептида (NT-proBNP). Результаты. По мере нарастания индекса массы миокарда левого желудочка (ИММЛЖ) отмечена тенденция к увеличению конечного систолического и диастолического размеров ЛЖ, сердечного индекса, объема левого предсердия, снижению ударного индекса без достоверных изменений объемных показателей ЛЖ, фракции выброса ЛЖ и давления в легочной артерии. По мере увеличения ГЛЖ выявлены достоверные различия по толщине межжелудочковой перегородки (ТМЖП) в диастолу (p multigroup – критерий множественного межгруппового сравнения – рmg<0,001) и частоте разных вариантов геометрии ЛЖ (рmg=0,016). Показатели спектра кровотока по легочным венам не имели достоверных различий при нарастании ГЛЖ. ИММЛЖ достоверно коррелировал с показателями соотношения максимальной скорости раннего диастолического наполнения и максимальной скорости предсердной систолы (r=0,521; р<0,001), и времени изоволюмического расслабления (r=-0,603; р=0,005). Увеличение ИММЛЖ было достоверно связано с увеличением уровня тканевого ингибитора матриксных металлопротеиназ (рmg=0,017), снижением показателя С-концевого телопептида проколлагена 1-го типа (рmg=0,011) и нарастанием NT-proBNP (рmg=0,010). Выводы. Увеличение ИММЛЖ у больных со стабильной стенокардией в сочетании с АГ при сохраненной фракции выброса ЛЖ ассоциируется с нарастанием тяжести диастолической дисфункции и формированием дилатации ЛЖ с преобладанием концентрической и увеличением частоты эксцентрической ГЛЖ. Степень выраженности ГЛЖ у больных со стабильной стенокардией в сочетании с АГ находится в прямой зависимости от уровня TIMP-1 и обратной зависимости от уровня С-концевого телопептида проколлагена 1-го типа в сыворотке крови. По мере увеличения ИММЛЖ нарастает уровень NT-proBNP, динамика которого может быть расценена как индикатор сердечно-сосудистого ремоделирования или как критерий развития хронической сердечной недостаточности с сохраненной фракцией выброса.
Ключевые слова: гипертрофия левого желудочка, дисфункция миокарда, коллагенолиз.
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Aim: to study some parameters of structural and functional condition of left ventricle myocardium in patients with II–III functional class of stable angina and arterial hypertension (AH) depending on left ventricle hypertrophy (LVH) evidence. Materials and methods: 90 patients with stable angina and AH and LVH were examined. The interconnections between frank of LVH and diastolic dysfunction, and serum levels of collagenolisis markers, and N-terminal peptide of brain natriuretic peptide (NT-proBNP) were evaluated. Results. There were tendencies for increase of LV terminal both systolic and diastolic sizes, cardiac index, left atrium volume during left ventricle myocardial mass index (LVMMI) was enlarged. There was tendency for decrease of stroke volume according to LVMMI increase, but there were no reliable changes in LV volumatic parameters, ejection fraction, and pulmonary artery pressure. There were reliable differences in interventricular septum diastolic thickness (рmg<0,001) and in frequency of LV geometry variants (рmg=0,016) according to LVMMI increase.
Parameters of pulmonary vein flow did not have any reliable changes during LVMMI increase. LVMMI has reliably correlated with E/A (r=0,521; р<0,001) and IVRT (r=-0,603; р=0,005). Also, LVMMI increase has reliably accompanied with both TIMP-1 and NT-proBNP increase (рmg=0,017, рmg=0,010, respectively), and CTP-I decrease (рmg=0,011). Conclusions. In patients with stable angina and AH with preserved ejection fraction LVMMI increase associates with worsening of diastolic dysfunction, LV dilatation with prevalence of concentric LVH and increase of frequency of eccentric LVH. In patients with stable angina and AH frank of LVH is in direct dependency with TIMP-1 serum level, and in indirect dependency with CTP-I. NT-proBNP has been increase during LVMMI grows, and it could be considered as cardiac-vascular remodeling indicator or as a criterion of CHF with preserved ejection fraction development.
Key words: left ventricle hypertrophy, myocardial dysfunction, collagenolisis.
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2. Desai CS, Ning H, Lloyd-Jones DM. Competing cardiovascular outcomes associated with electrocardiographic left ventricular hypertrophy: the Atherosclerosis Risk in Communities Study. Heart 2012; 98 (4): 330–4.
3. Salvetti M, Muiesan ML, Paini A et al. Left ventricular hypertrophy and renal dysfunction during antihypertensive treatment adversely affect cardiovascular prognosis in hypertensive patients. J Hypertens 2012; 30 (2): 411–20.
4. Vilahur G, Juan-Babot O, Peña E et al. Molecular and cellular mechanisms involved in cardiac remodeling after acute myocardial infarction. J Mol Cell Cardiol 2011; 50 (3): 522–33.
5. Dixon JA, Spinale FG. Myocardial remodeling: cellular and extracellular events and targets. Annu Rev Physiol 2011; 73: 47–68.
6. Gajarsa JJ, Kloner RA. Left ventricular remodeling in the post-infarction heart: a review of cellular, molecular mechanisms, and therapeutic modalities. Heart Fail Rev 2011; 16 (1): 13–21.
7. Briasoulis A, Tousoulis D, Papageorgiou N et al. Novel therapeutic approaches targeting matrix metalloproteinases in cardiovascular disease. Curr Top Med Chem 2012; 12 (10): 1214–21.
8. Galderisi M. Diagnosis and management of left ventricular diastolic dysfunction in the hypertensive patient. Am J Hypertens 2011; 24 (5): 507–17.
9. Azevedo PS, Polegato BF, Minicucci MF et al. Early echocardiographic predictors of increased left ventricular end-diastolic pressure three months after myocardial infarction in rats. Med Sci Monit 2012; 18 (7): BR253–8.
10. Krishnamoorthy A, Brown T, Ayers CR et al. Progression from normal to reduced left ventricular ejection fraction in patients with concentric left ventricular hypertrophy after long-term follow-up. Am J Cardiol 2011; 108 (7): 997–1001.
11. Milani RV, Drazner MH, Lavie CJ et al. Progression from concentric left ventricular hypertrophy and normal ejection fraction to left ventricular dysfunction. Am J Cardiol 2011; 108 (7): 992–6.
12. Faul C. Fibroblast growth factor 23 and the heart. Curr Opin Nephrol Hypertens 2012; 21 (4): 369–75.
13. Andersen MJ, Ersbøll M, Bro-Jeppesen J et al. Exercise hemodynamics in patients with and without diastolic dysfunction and preserved ejection fraction after myocardial infarction.Circ Heart Fail 2012; 5 (4): 444–51.
14. Moon J, Rim SJ, Cho IJ et al. Left ventricular hypertrophy determines the severity of diastolic dysfunction in patients with nonvalvular atrial fibrillation and preserved left ventricular systolic function. Clin Exp Hypertens 2010; 32 (8): 540–6.
15. Fontana V, Silva PS, Gerlach RF, Tanus-Santos JE. Circulating matrix metalloproteinases and their inhibitors in hypertension. Clin Chim Acta 2012; 413 (7–8): 656–62.
16. Benjamin MM, Khalil RA. Matrix metalloproteinase inhibitors as investigative tools in the pathogenesis and management of vascular disease. EXS 2012; 103: 209–79.
17. Marchesi C, Dentali F, Nicolini E et al. Plasma levels of matrix metalloproteinases and their inhibitors in hypertension: a systematic review and meta-analysis. J Hypertens 2012; 30 (1): 3–16.
18. Irzmanski R, Barylski M, Banach M et al. The concentration of atrial and brain natriuretic peptide in patients with idiopathic hypertension. Med Sci Monit 2007; 13 (10): CR449–56.
19. Elmas E, Brueckmann M, Lang S et al. Midregional pro-atrial natriuretic peptide is a useful indicator for the detection of impaired left ventricular function in patients with coronary artery disease. Int J Cardiol 2008; 128 (2): 244–9.
20. Zhong-Ling Z, Jing-Yuan M. Research Advances in B-type Natriuretic Peptide and Its Clinical Application in the Patients with Cardiovascular Diseases. Zhongguo Yi Xue Ke Xue Yuan Xue Bao 2012; 34 (2): 183–9.
________________________________________________
1. Berkin KE, Ball SG. Essential hypertension: the heart and hypertension. Hypertension 2001; 86: 467–75.
2. Desai CS, Ning H, Lloyd-Jones DM. Competing cardiovascular outcomes associated with electrocardiographic left ventricular hypertrophy: the Atherosclerosis Risk in Communities Study. Heart 2012; 98 (4): 330–4.
3. Salvetti M, Muiesan ML, Paini A et al. Left ventricular hypertrophy and renal dysfunction during antihypertensive treatment adversely affect cardiovascular prognosis in hypertensive patients. J Hypertens 2012; 30 (2): 411–20.
4. Vilahur G, Juan-Babot O, Peña E et al. Molecular and cellular mechanisms involved in cardiac remodeling after acute myocardial infarction. J Mol Cell Cardiol 2011; 50 (3): 522–33.
5. Dixon JA, Spinale FG. Myocardial remodeling: cellular and extracellular events and targets. Annu Rev Physiol 2011; 73: 47–68.
6. Gajarsa JJ, Kloner RA. Left ventricular remodeling in the post-infarction heart: a review of cellular, molecular mechanisms, and therapeutic modalities. Heart Fail Rev 2011; 16 (1): 13–21.
7. Briasoulis A, Tousoulis D, Papageorgiou N et al. Novel therapeutic approaches targeting matrix metalloproteinases in cardiovascular disease. Curr Top Med Chem 2012; 12 (10): 1214–21.
8. Galderisi M. Diagnosis and management of left ventricular diastolic dysfunction in the hypertensive patient. Am J Hypertens 2011; 24 (5): 507–17.
9. Azevedo PS, Polegato BF, Minicucci MF et al. Early echocardiographic predictors of increased left ventricular end-diastolic pressure three months after myocardial infarction in rats. Med Sci Monit 2012; 18 (7): BR253–8.
10. Krishnamoorthy A, Brown T, Ayers CR et al. Progression from normal to reduced left ventricular ejection fraction in patients with concentric left ventricular hypertrophy after long-term follow-up. Am J Cardiol 2011; 108 (7): 997–1001.
11. Milani RV, Drazner MH, Lavie CJ et al. Progression from concentric left ventricular hypertrophy and normal ejection fraction to left ventricular dysfunction. Am J Cardiol 2011; 108 (7): 992–6.
12. Faul C. Fibroblast growth factor 23 and the heart. Curr Opin Nephrol Hypertens 2012; 21 (4): 369–75.
13. Andersen MJ, Ersbøll M, Bro-Jeppesen J et al. Exercise hemodynamics in patients with and without diastolic dysfunction and preserved ejection fraction after myocardial infarction.Circ Heart Fail 2012; 5 (4): 444–51.
14. Moon J, Rim SJ, Cho IJ et al. Left ventricular hypertrophy determines the severity of diastolic dysfunction in patients with nonvalvular atrial fibrillation and preserved left ventricular systolic function. Clin Exp Hypertens 2010; 32 (8): 540–6.
15. Fontana V, Silva PS, Gerlach RF, Tanus-Santos JE. Circulating matrix metalloproteinases and their inhibitors in hypertension. Clin Chim Acta 2012; 413 (7–8): 656–62.
16. Benjamin MM, Khalil RA. Matrix metalloproteinase inhibitors as investigative tools in the pathogenesis and management of vascular disease. EXS 2012; 103: 209–79.
17. Marchesi C, Dentali F, Nicolini E et al. Plasma levels of matrix metalloproteinases and their inhibitors in hypertension: a systematic review and meta-analysis. J Hypertens 2012; 30 (1): 3–16.
18. Irzmanski R, Barylski M, Banach M et al. The concentration of atrial and brain natriuretic peptide in patients with idiopathic hypertension. Med Sci Monit 2007; 13 (10): CR449–56.
19. Elmas E, Brueckmann M, Lang S et al. Midregional pro-atrial natriuretic peptide is a useful indicator for the detection of impaired left ventricular function in patients with coronary artery disease. Int J Cardiol 2008; 128 (2): 244–9.
20. Zhong-Ling Z, Jing-Yuan M. Research Advances in B-type Natriuretic Peptide and Its Clinical Application in the Patients with Cardiovascular Diseases. Zhongguo Yi Xue Ke Xue Yuan Xue Bao 2012; 34 (2): 183–9.