Editorial Comment
The importance of left ventricular geometry in hypertensive heart disease Thomas Kahan and Hans Persson
See original paper on page 745
S
igns of hypertensive heart disease are early and important findings in patients with hypertension, and may have direct pathophysiological implications in the progression from early hypertension to cardiovascular morbidity and mortality [1,2]. There are several determinants for the development of left ventricular hypertrophy. Haemodynamic factors such as blood pressure, large artery structure and stiffness, and volume load are important. Also nonhaemodynamic mechanisms such as trophic factors mediated by the sympathetic nervous system, the renin–angiotensin–aldosterone system, and other neurohormonal mediators play an important role in the development of left ventricular hypertrophy [3]. Aside from the accelerated atherosclerotic process of coronary artery disease by elevated blood pressure, cardiac hypertrophy will cause microcirculatory alterations and impaired coronary flow reserve, and promote myocardial ischemia in hypertensive heart disease. An increased afterload will also induce cardiomyocyte hypertrophy, stimulate fibroblasts and increase collagen formation, and cause remodelling of the myocardium with an increase in myocardial fibrosis. Cardiomyocyte hypertrophy will impair systolic contractility and diastolic filling, causing left ventricular systolic and diastolic dysfunction. Myocardial fibrosis will contribute to impaired coronary flow reserve and diastolic dysfunction, and will alter electrical conduction properties with an increased risk for arrhythmias [4–6]. It has long been established that left ventricular hypertrophy by electrocardiography is a strong and independent risk factor for cardiovascular morbidity and mortality, and all-cause mortality in the general population and in patients with hypertension or coronary artery disease [7,8]. Of note, left ventricular hypertrophy can occur through wall thickening or chamber dilatation, and determination of left ventricular mass by echocardiography or MRI techniques
Journal of Hypertension 2015, 33:690–692 Division of Cardiovascular Medicine, Department of Clinical Sciences, Danderyd Hospital, Karolinska Institutet and Department of Cardiology, Danderyd University Hospital Corporation, Stockholm, Sweden Correspondence to Prof Thomas Kahan, Department of Cardiology, Danderyd University Hospital Corporation, S-182 88 Stockholm, Sweden. Tel: +46 8 123 568 61; fax: +46 8 755 0868; e-mail: [email protected] J Hypertens 33:690–692 Copyright ß 2015 Wolters Kluwer Health, Inc. All rights reserved. DOI:10.1097/HJH.0000000000000557
690
www.jhypertension.com
gives superior sensitivity and can provide additional important information. Using echocardiography, four distinct patterns of left ventricular geometry in hypertensive patients based on left ventricular geometric remodelling and hypertrophy was first described some 25 years ago: normal left ventricular geometry and mass, left ventricular remodelling (with increased relative wall thickness and normal left ventricular mass), eccentric left ventricular hypertrophy, and concentric left ventricular hypertrophy [9]. It was subsequently demonstrated that long-term cardiovascular morbidity and all-cause mortality were associated with the left ventricular geometric pattern and were lowest in patients with normal left ventricular geometry, and progressively worse with left ventricular concentric remodelling, eccentric left ventricular hypertrophy, and concentric left ventricular hypertrophy [10,11]. One limitation of the classification into eccentric or concentric left ventricular hypertrophy is that it depends on the ratio of wall thickness to left ventricular dilatation, rather than the independent changes of these two measures. This and other considerations recently led Khouri et al. [12] to suggest a new classification into four groups of left ventricular hypertrophy, in which both left ventricular concentricity and volume were taken into consideration. Their results suggested that eccentric left ventricular hypertrophy with no dilatation appeared to provide a lower risk for coronary artery disease and myocardial function impairment than patients in the remaining three groups of cardiac hypertrophy. However, this cross-sectional study did not have results on outcome, and the potential prognostic information from this proposed classification of left ventricular hypertrophy remained to be demonstrated [13]. De Simone et al. [13] now report results in the Journal of Hypertension, which extend our knowledge and understanding of hypertensive left ventricular geometric abnormalities as a risk factor for cardiovascular morbidity and mortality. The authors investigated 8848 treated hypertensive patients without other significant cardiovascular disease, attending general practitioners and community hospitals within an open registry (Campania Salute Network) in Southern Italy. Mean age was 53 years, 44% were women, and obesity was present in 42% and diabetes in 11%. All patients were initially investigated by echocardiography, and incident cases of a composite outcome of Volume 33 Number 4 April 2015
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
The heart in hypertension
nonfatal and fatal myocardial infarction, stroke, and sudden death during a median follow-up of 35 months ware evaluated. Normal left ventricular geometry was present in 66%; concentric remodelling in 5%; and eccentric nondilated, eccentric dilated, concentric nondilated, and concentric dilated left ventricular hypertrophy in 20, 4, 5, and less than 1%, respectively. Of note, obesity was most prevalent among patients with dilated left ventricular hypertrophy forms, and close to one-third with dilated concentric left ventricular hypertrophy had diabetes. Compared with hypertensive patients with normal left ventricular geometry, the hazard ratios for a fatal or nonfatal cardiovascular event increased progressively from concentric left ventricular remodelling through eccentric nondilated, eccentric dilated, concentric nondilated to concentric dilated (hazard ratios with 95% confidence intervals): 1.20 [0.80–1.60], 1.23 [0.87–1.74], 1.95 [1.22–3.12], 2.16 [1.23–3.80], and 8.91 [2.17–36.59]. Further analyses showed that left ventricular mass indexed for body size was the key parameter for future cardiovascular risk as there is an association between left ventricular mass and geometric pattern. These important results by de Simone et al. [13] confirm recent findings in a smaller group of 939 patients with hypertension-induced left ventricular hypertrophy by ECG within the Losartan intervention for endpoint reduction study [14]. This suggests that the extent of both pressure overload and volume overload may be associated with the risk for future cardiovascular events (Fig. 1). Whether these alterations in haemodynamic overload in hypertension should be addressed by tailored antihypertensive drug therapy in an individual patient to improve prognosis cannot be answered by the results presented by de Simone et al. [13], but warrant further study. Hypertension is a major etiologic risk factor for the development of heart failure and confers the greatest attributable risk [15]. Thus, identification of high-risk
Normal left ventricular mass
hypertensive patients and the appropriate control of blood pressure control may prevent the development of heart failure. However, the mechanisms for the transition from hypertension through hypertensive heart disease to heart failure and fatality are not fully understood. Echocardiographic indices of diastolic dysfunction in hypertension and in heart failure with preserved left ventricular ejections fraction are related to the extent of myocardial fibrosis, which is assessed by circulating biomarkers of myocardial collagen turnover [16,17]. These findings also occur in hypertensive patients with normal left ventricular geometry and mass, suggesting that myocardial fibrosis may precede the development of hypertension-induced left ventricular hypertrophy [16]. Animal experiments suggest that left ventricular remodelling with dilatation is more deleterious than depressed myocardial function to predict the development of heart failure in pressure overload induced left ventricular hypertrophy [18]. The echocardiographic substudy of the Candesartan in heart failure: Assessment of reduction in mortality and morbidity-preserved study (CHARMES) investigated 312 patients with chronic heart failure and preserved left ventricular systolic function; 68% were hypertensive, 52% had left ventricular hypertrophy, and 67% diastolic dysfunction [19]. We found that diastolic dysfunction is an important independent predictor of adverse outcome during a median follow-up time of 19 months. Elevated biomarkers of myocardial collagen type I in hypertension-induced heart failure with reduced left ventricular ejection fraction are related to the amount of myocardial collagen content, and augmented degradation of myocardial collagen scaffold may exacerbate heart failure by left ventricular dilatation and impaired contractile function [20]. In chronic heart failure with reduced left ventricular ejection fraction we found biomarkers of collagen type I synthesis and degradation independently related
Normal
Normal
Concentric remodelling
Concentric remodelling
Eccentric hypertrophy Dilated eccentric Left ventricular hypertrophy Nondilated concentric Concentric hypertrophy Dilated concentric
Risk for cardiovascular event
Nondilated eccentric
FIGURE 1 Schematic illustration of different left ventricular patterns in hypertensive patients, and their relation to the risk for a future cardiovascular nonfatal or fatal event. Based on results from [12–14].
Journal of Hypertension
www.jhypertension.com
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
691
Kahan and Persson
to brain natriuretic peptide and to indices of left ventricular dimension and diastolic function [21]. Our preliminary observations in heart failure patients with reduced left ventricular ejection function suggest that disturbances of collagen type I metabolism may be involved in cardiac structural and functional remodelling, and have prognostic implications. In particular, an increased turnover of collagen type I appears to be related to cardiovascular mortality. We have proposed that brain natriuretic peptide may contribute to alterations of collagen type I metabolism and that brain natriuretic peptide under some circumstances may have antifibrotic effects by an increased degradation of myocardial collagen type I fibres, [21]. Taken together, there may be a link between increased myocardial collagen degradation, left ventricular dilatation, and unfavourable prognosis. Thus, temporal changes of myocardial collagen metabolism during the progression of heart failure and the prognostic impact of these biomarkers in heart failure with preserved or reduced left ventricular ejection fraction warrant further study. In this context, it would be interesting to examine circulating biomarkers of myocardial collagen in relation to the proposed new classification of hypertensive left ventricular geometric abnormalities [12,13] to assess disturbances of collagen metabolism leading to alterations in the myocardial collagen network. Such information may help us to better understand the dynamic changes in myocardial extracellular matrix composition in relation to changes in left ventricular geometry. This could improve our understanding of the transition from hypertension to heart failure and may point toward the new diagnostic and therapeutic directions. There are some potential limitations to the study by de Simone et al. [13]. The study is based on an open registry collecting data from general practitioners and community hospitals and may be subject to selection bias. Concentric dilated left ventricular hypertrophy was present in only 13 of 8848 included hypertensive patients, and conclusions about this left ventricular geometric abnormality may be uncertain. Nevertheless, the relations between left ventricular geometric pattern and predicted risk appear to support earlier observations [12,14], In conclusion, it is important to identify patients with hypertensive heart disease early, as antihypertensive treatment will reduce the risk for future cardiovascular complications. The study by de Simone et al. [13] demonstrates that a new classification of hypertensive left ventricular geometric abnormalities in which left ventricular mass and dilatation are given full consideration appears to improve risk stratification. The potential clinical benefit of an improved risk assessment and appropriate treatment of hypertensive patients may be considerable.
ACKNOWLEDGEMENTS Conflicts of interest There are no conflicts of interest.
692
www.jhypertension.com
REFERENCES 1. Dzau V, Braunwald E. Resolved and unresolved issues in the prevention and treatment of coronary artery disease: a workshop consensus statement. Am Heart J 1991; 121:1244–1263. 2. O’Rourke MF, Safar ME, Dzau V. The cardiovascular continuum extended: aging effects on the aorta and microvasculature. Vasc Med 2010; 15:461–468. 3. Kahan T. The importance of myocardial fibrosis in hypertensive heart disease. J Hypertens 2012; 30:685–687. 4. Kahan T, Bergfeldt L. Left ventricular hypertrophy in hypertension: tsI arrhythmogenic potential. Heart 2005; 91:250–256. 5. Dı´ez J, Frohlich ED. A translational approach to hypertensive heart disease. Hypertension 2010; 55:1–8. 6. Lo¨fsjo¨ga˚rd J, Persson H, Dı´ez J, Lo´pez B, Gonza´lez A, Edner M, et al. Atrial fibrillation and biomarkers of myocardial fibrosis in heart failure. Scand Cardiovasc J 2014; 15:463–469. 7. Kannel WB, Gordon T, Offutt D. Left ventricular hypertrophy by electrocardiogram: prevalence, incidence, and mortality in the Framingham Study. Ann Intern Med 1969; 71:89–105. 8. Kannel WB, Castelli WP, McNamara PM, McKee PA, Feinleib M. Role of blood pressure in the development of congestive heart failure. The Framingham study. N Engl J Med 1972; 287:781–787. 9. Ganau A, Devereux RB, Roman MJ, de Simone G, Pickering TG, Saba PS, et al. Patterns of left ventricular hypertrophy and geometric modelling is essential hypertension. J Am Coll Cardiol 1992; 19:1550–1558. 10. Koren MJ1, Devereux RB, Casale PN, Savage DD, Laragh JH. Relation of left ventricular and geometry to morbidity and mortality in uncomplicated essential hypertension. Ann Intern Med 1991; 114:345–352. 11. Krumholz HM, Larson M, Levy D. Prognosis of left ventricular geometric patterns in the Framingham heart study. J Am Coll Cardiol 1995; 25:879–884. 12. Khouri MG, Peshock RM, Ayers CR, de Lemos JA, Drazner MH. A 4-tiered classification of left ventricular hypertrophy based on left ventricular geometry: the Dallas heart study. Circ Cardiovasc Imaging 2010; 3:164–171. 13. de Simone G, Izzo R, Aurigemma GP, De Marco M, Rozza F, Trimarco V, et al. Cardiovascular risk in relation to a new classification of hypertensive left ventricular geometric abnormalities. J Hypertens 2015; 33:745–754. 14. Bang CN, Gerdts E, Aurigemma GP, Boman K, de Simone G, Dahlo¨f B, et al. Four-group classification of left ventricular hypertrophy based on ventricular concentricity and dilatation identifies a low-risk subset of eccentric hypertrophy in hypertensive patients. Circ Cardiovasc Imaging 2014; 7:422–429. 15. Levy D, Larson MG, Vasan RS, Kannel WB, Ho KK. The progression from hypertension to congestive heart failure. JAMA 1996; 275:1557– 1562. 16. Mu¨ller-Brunotte R, Kahan T, Lo´pez B, Edner M, Gonza`les R, Dı´ez J, Malmqvist M. Myocardial fibrosis and diastolic dysfunction in hypertensive patients. J Hypertens 2007; 25:1967–1973. 17. Martos R, Baugh J, Ledwidge M, O’Loughlin C, Conlon C, Patle A, et al. Diastolic heart failure: evidence of increased myocardial collagen turnover linked to diastolic dysfunction. Circulation 2007; 115:888– 895. 18. Norton GR, Woodiwiss AJ, Gaasch WH, Mela T, Chung ES, Aurigemma GP, Meyer TE. Heart failure in pressure overload hypertrophy. The relative roles of ventricular remodeling and myocardial dysfunction. J Am Coll Cardiol 2002; 39:664–671. 19. Persson H, Lonn E, Edner M, Baruch L, Lang CC, Morton JJ, et al. Diastolic dysfunction in heart failure with preserved systolic function: need for objective evidence: results from the CHARM Echocardiographic Substudy – CHARMES. J Am Coll Cardiol 2007; 49:687–694. 20. Querejeta R, Lo´pez B, Gonza´lez A, Sanchez E, Larman M, Martinez Ubago JL, et al. Increased collagen type i synthesis in patients with heart failure of hypertensive origin: relation to myocardial fibrosis. Circulation 2004; 110:1263–1268. 21. Lo¨fsjo¨ga˚rd J, Kahan T, Dı´ez J, Lo´pez B, Gonza´lez A, Edner M, et al. Biomarkers of collagen type I metabolism are related to BNP, left ventricular size and diastolic function in heart failure. J Cardiovasc Med 2014; 15:463–469.
Volume 33 Number 4 April 2015
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
The importance of left ventricular geometry in hypertensive heart disease Thomas Kahan and Hans Persson
See original paper on page 745
S
igns of hypertensive heart disease are early and important findings in patients with hypertension, and may have direct pathophysiological implications in the progression from early hypertension to cardiovascular morbidity and mortality [1,2]. There are several determinants for the development of left ventricular hypertrophy. Haemodynamic factors such as blood pressure, large artery structure and stiffness, and volume load are important. Also nonhaemodynamic mechanisms such as trophic factors mediated by the sympathetic nervous system, the renin–angiotensin–aldosterone system, and other neurohormonal mediators play an important role in the development of left ventricular hypertrophy [3]. Aside from the accelerated atherosclerotic process of coronary artery disease by elevated blood pressure, cardiac hypertrophy will cause microcirculatory alterations and impaired coronary flow reserve, and promote myocardial ischemia in hypertensive heart disease. An increased afterload will also induce cardiomyocyte hypertrophy, stimulate fibroblasts and increase collagen formation, and cause remodelling of the myocardium with an increase in myocardial fibrosis. Cardiomyocyte hypertrophy will impair systolic contractility and diastolic filling, causing left ventricular systolic and diastolic dysfunction. Myocardial fibrosis will contribute to impaired coronary flow reserve and diastolic dysfunction, and will alter electrical conduction properties with an increased risk for arrhythmias [4–6]. It has long been established that left ventricular hypertrophy by electrocardiography is a strong and independent risk factor for cardiovascular morbidity and mortality, and all-cause mortality in the general population and in patients with hypertension or coronary artery disease [7,8]. Of note, left ventricular hypertrophy can occur through wall thickening or chamber dilatation, and determination of left ventricular mass by echocardiography or MRI techniques
Journal of Hypertension 2015, 33:690–692 Division of Cardiovascular Medicine, Department of Clinical Sciences, Danderyd Hospital, Karolinska Institutet and Department of Cardiology, Danderyd University Hospital Corporation, Stockholm, Sweden Correspondence to Prof Thomas Kahan, Department of Cardiology, Danderyd University Hospital Corporation, S-182 88 Stockholm, Sweden. Tel: +46 8 123 568 61; fax: +46 8 755 0868; e-mail: [email protected] J Hypertens 33:690–692 Copyright ß 2015 Wolters Kluwer Health, Inc. All rights reserved. DOI:10.1097/HJH.0000000000000557
690
www.jhypertension.com
gives superior sensitivity and can provide additional important information. Using echocardiography, four distinct patterns of left ventricular geometry in hypertensive patients based on left ventricular geometric remodelling and hypertrophy was first described some 25 years ago: normal left ventricular geometry and mass, left ventricular remodelling (with increased relative wall thickness and normal left ventricular mass), eccentric left ventricular hypertrophy, and concentric left ventricular hypertrophy [9]. It was subsequently demonstrated that long-term cardiovascular morbidity and all-cause mortality were associated with the left ventricular geometric pattern and were lowest in patients with normal left ventricular geometry, and progressively worse with left ventricular concentric remodelling, eccentric left ventricular hypertrophy, and concentric left ventricular hypertrophy [10,11]. One limitation of the classification into eccentric or concentric left ventricular hypertrophy is that it depends on the ratio of wall thickness to left ventricular dilatation, rather than the independent changes of these two measures. This and other considerations recently led Khouri et al. [12] to suggest a new classification into four groups of left ventricular hypertrophy, in which both left ventricular concentricity and volume were taken into consideration. Their results suggested that eccentric left ventricular hypertrophy with no dilatation appeared to provide a lower risk for coronary artery disease and myocardial function impairment than patients in the remaining three groups of cardiac hypertrophy. However, this cross-sectional study did not have results on outcome, and the potential prognostic information from this proposed classification of left ventricular hypertrophy remained to be demonstrated [13]. De Simone et al. [13] now report results in the Journal of Hypertension, which extend our knowledge and understanding of hypertensive left ventricular geometric abnormalities as a risk factor for cardiovascular morbidity and mortality. The authors investigated 8848 treated hypertensive patients without other significant cardiovascular disease, attending general practitioners and community hospitals within an open registry (Campania Salute Network) in Southern Italy. Mean age was 53 years, 44% were women, and obesity was present in 42% and diabetes in 11%. All patients were initially investigated by echocardiography, and incident cases of a composite outcome of Volume 33 Number 4 April 2015
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
The heart in hypertension
nonfatal and fatal myocardial infarction, stroke, and sudden death during a median follow-up of 35 months ware evaluated. Normal left ventricular geometry was present in 66%; concentric remodelling in 5%; and eccentric nondilated, eccentric dilated, concentric nondilated, and concentric dilated left ventricular hypertrophy in 20, 4, 5, and less than 1%, respectively. Of note, obesity was most prevalent among patients with dilated left ventricular hypertrophy forms, and close to one-third with dilated concentric left ventricular hypertrophy had diabetes. Compared with hypertensive patients with normal left ventricular geometry, the hazard ratios for a fatal or nonfatal cardiovascular event increased progressively from concentric left ventricular remodelling through eccentric nondilated, eccentric dilated, concentric nondilated to concentric dilated (hazard ratios with 95% confidence intervals): 1.20 [0.80–1.60], 1.23 [0.87–1.74], 1.95 [1.22–3.12], 2.16 [1.23–3.80], and 8.91 [2.17–36.59]. Further analyses showed that left ventricular mass indexed for body size was the key parameter for future cardiovascular risk as there is an association between left ventricular mass and geometric pattern. These important results by de Simone et al. [13] confirm recent findings in a smaller group of 939 patients with hypertension-induced left ventricular hypertrophy by ECG within the Losartan intervention for endpoint reduction study [14]. This suggests that the extent of both pressure overload and volume overload may be associated with the risk for future cardiovascular events (Fig. 1). Whether these alterations in haemodynamic overload in hypertension should be addressed by tailored antihypertensive drug therapy in an individual patient to improve prognosis cannot be answered by the results presented by de Simone et al. [13], but warrant further study. Hypertension is a major etiologic risk factor for the development of heart failure and confers the greatest attributable risk [15]. Thus, identification of high-risk
Normal left ventricular mass
hypertensive patients and the appropriate control of blood pressure control may prevent the development of heart failure. However, the mechanisms for the transition from hypertension through hypertensive heart disease to heart failure and fatality are not fully understood. Echocardiographic indices of diastolic dysfunction in hypertension and in heart failure with preserved left ventricular ejections fraction are related to the extent of myocardial fibrosis, which is assessed by circulating biomarkers of myocardial collagen turnover [16,17]. These findings also occur in hypertensive patients with normal left ventricular geometry and mass, suggesting that myocardial fibrosis may precede the development of hypertension-induced left ventricular hypertrophy [16]. Animal experiments suggest that left ventricular remodelling with dilatation is more deleterious than depressed myocardial function to predict the development of heart failure in pressure overload induced left ventricular hypertrophy [18]. The echocardiographic substudy of the Candesartan in heart failure: Assessment of reduction in mortality and morbidity-preserved study (CHARMES) investigated 312 patients with chronic heart failure and preserved left ventricular systolic function; 68% were hypertensive, 52% had left ventricular hypertrophy, and 67% diastolic dysfunction [19]. We found that diastolic dysfunction is an important independent predictor of adverse outcome during a median follow-up time of 19 months. Elevated biomarkers of myocardial collagen type I in hypertension-induced heart failure with reduced left ventricular ejection fraction are related to the amount of myocardial collagen content, and augmented degradation of myocardial collagen scaffold may exacerbate heart failure by left ventricular dilatation and impaired contractile function [20]. In chronic heart failure with reduced left ventricular ejection fraction we found biomarkers of collagen type I synthesis and degradation independently related
Normal
Normal
Concentric remodelling
Concentric remodelling
Eccentric hypertrophy Dilated eccentric Left ventricular hypertrophy Nondilated concentric Concentric hypertrophy Dilated concentric
Risk for cardiovascular event
Nondilated eccentric
FIGURE 1 Schematic illustration of different left ventricular patterns in hypertensive patients, and their relation to the risk for a future cardiovascular nonfatal or fatal event. Based on results from [12–14].
Journal of Hypertension
www.jhypertension.com
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
691
Kahan and Persson
to brain natriuretic peptide and to indices of left ventricular dimension and diastolic function [21]. Our preliminary observations in heart failure patients with reduced left ventricular ejection function suggest that disturbances of collagen type I metabolism may be involved in cardiac structural and functional remodelling, and have prognostic implications. In particular, an increased turnover of collagen type I appears to be related to cardiovascular mortality. We have proposed that brain natriuretic peptide may contribute to alterations of collagen type I metabolism and that brain natriuretic peptide under some circumstances may have antifibrotic effects by an increased degradation of myocardial collagen type I fibres, [21]. Taken together, there may be a link between increased myocardial collagen degradation, left ventricular dilatation, and unfavourable prognosis. Thus, temporal changes of myocardial collagen metabolism during the progression of heart failure and the prognostic impact of these biomarkers in heart failure with preserved or reduced left ventricular ejection fraction warrant further study. In this context, it would be interesting to examine circulating biomarkers of myocardial collagen in relation to the proposed new classification of hypertensive left ventricular geometric abnormalities [12,13] to assess disturbances of collagen metabolism leading to alterations in the myocardial collagen network. Such information may help us to better understand the dynamic changes in myocardial extracellular matrix composition in relation to changes in left ventricular geometry. This could improve our understanding of the transition from hypertension to heart failure and may point toward the new diagnostic and therapeutic directions. There are some potential limitations to the study by de Simone et al. [13]. The study is based on an open registry collecting data from general practitioners and community hospitals and may be subject to selection bias. Concentric dilated left ventricular hypertrophy was present in only 13 of 8848 included hypertensive patients, and conclusions about this left ventricular geometric abnormality may be uncertain. Nevertheless, the relations between left ventricular geometric pattern and predicted risk appear to support earlier observations [12,14], In conclusion, it is important to identify patients with hypertensive heart disease early, as antihypertensive treatment will reduce the risk for future cardiovascular complications. The study by de Simone et al. [13] demonstrates that a new classification of hypertensive left ventricular geometric abnormalities in which left ventricular mass and dilatation are given full consideration appears to improve risk stratification. The potential clinical benefit of an improved risk assessment and appropriate treatment of hypertensive patients may be considerable.
ACKNOWLEDGEMENTS Conflicts of interest There are no conflicts of interest.
692
www.jhypertension.com
REFERENCES 1. Dzau V, Braunwald E. Resolved and unresolved issues in the prevention and treatment of coronary artery disease: a workshop consensus statement. Am Heart J 1991; 121:1244–1263. 2. O’Rourke MF, Safar ME, Dzau V. The cardiovascular continuum extended: aging effects on the aorta and microvasculature. Vasc Med 2010; 15:461–468. 3. Kahan T. The importance of myocardial fibrosis in hypertensive heart disease. J Hypertens 2012; 30:685–687. 4. Kahan T, Bergfeldt L. Left ventricular hypertrophy in hypertension: tsI arrhythmogenic potential. Heart 2005; 91:250–256. 5. Dı´ez J, Frohlich ED. A translational approach to hypertensive heart disease. Hypertension 2010; 55:1–8. 6. Lo¨fsjo¨ga˚rd J, Persson H, Dı´ez J, Lo´pez B, Gonza´lez A, Edner M, et al. Atrial fibrillation and biomarkers of myocardial fibrosis in heart failure. Scand Cardiovasc J 2014; 15:463–469. 7. Kannel WB, Gordon T, Offutt D. Left ventricular hypertrophy by electrocardiogram: prevalence, incidence, and mortality in the Framingham Study. Ann Intern Med 1969; 71:89–105. 8. Kannel WB, Castelli WP, McNamara PM, McKee PA, Feinleib M. Role of blood pressure in the development of congestive heart failure. The Framingham study. N Engl J Med 1972; 287:781–787. 9. Ganau A, Devereux RB, Roman MJ, de Simone G, Pickering TG, Saba PS, et al. Patterns of left ventricular hypertrophy and geometric modelling is essential hypertension. J Am Coll Cardiol 1992; 19:1550–1558. 10. Koren MJ1, Devereux RB, Casale PN, Savage DD, Laragh JH. Relation of left ventricular and geometry to morbidity and mortality in uncomplicated essential hypertension. Ann Intern Med 1991; 114:345–352. 11. Krumholz HM, Larson M, Levy D. Prognosis of left ventricular geometric patterns in the Framingham heart study. J Am Coll Cardiol 1995; 25:879–884. 12. Khouri MG, Peshock RM, Ayers CR, de Lemos JA, Drazner MH. A 4-tiered classification of left ventricular hypertrophy based on left ventricular geometry: the Dallas heart study. Circ Cardiovasc Imaging 2010; 3:164–171. 13. de Simone G, Izzo R, Aurigemma GP, De Marco M, Rozza F, Trimarco V, et al. Cardiovascular risk in relation to a new classification of hypertensive left ventricular geometric abnormalities. J Hypertens 2015; 33:745–754. 14. Bang CN, Gerdts E, Aurigemma GP, Boman K, de Simone G, Dahlo¨f B, et al. Four-group classification of left ventricular hypertrophy based on ventricular concentricity and dilatation identifies a low-risk subset of eccentric hypertrophy in hypertensive patients. Circ Cardiovasc Imaging 2014; 7:422–429. 15. Levy D, Larson MG, Vasan RS, Kannel WB, Ho KK. The progression from hypertension to congestive heart failure. JAMA 1996; 275:1557– 1562. 16. Mu¨ller-Brunotte R, Kahan T, Lo´pez B, Edner M, Gonza`les R, Dı´ez J, Malmqvist M. Myocardial fibrosis and diastolic dysfunction in hypertensive patients. J Hypertens 2007; 25:1967–1973. 17. Martos R, Baugh J, Ledwidge M, O’Loughlin C, Conlon C, Patle A, et al. Diastolic heart failure: evidence of increased myocardial collagen turnover linked to diastolic dysfunction. Circulation 2007; 115:888– 895. 18. Norton GR, Woodiwiss AJ, Gaasch WH, Mela T, Chung ES, Aurigemma GP, Meyer TE. Heart failure in pressure overload hypertrophy. The relative roles of ventricular remodeling and myocardial dysfunction. J Am Coll Cardiol 2002; 39:664–671. 19. Persson H, Lonn E, Edner M, Baruch L, Lang CC, Morton JJ, et al. Diastolic dysfunction in heart failure with preserved systolic function: need for objective evidence: results from the CHARM Echocardiographic Substudy – CHARMES. J Am Coll Cardiol 2007; 49:687–694. 20. Querejeta R, Lo´pez B, Gonza´lez A, Sanchez E, Larman M, Martinez Ubago JL, et al. Increased collagen type i synthesis in patients with heart failure of hypertensive origin: relation to myocardial fibrosis. Circulation 2004; 110:1263–1268. 21. Lo¨fsjo¨ga˚rd J, Kahan T, Dı´ez J, Lo´pez B, Gonza´lez A, Edner M, et al. Biomarkers of collagen type I metabolism are related to BNP, left ventricular size and diastolic function in heart failure. J Cardiovasc Med 2014; 15:463–469.
Volume 33 Number 4 April 2015
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
