In order to bring you the best possible user experience, this site uses Javascript. If you are seeing this message, it is likely that the Javascript option in your browser is disabled. For optimal viewing of this site, please ensure that Javascript is enabled for your browser.
Did you know that your browser is out of date? To get the best experience using our website we recommend that you upgrade to a newer version. Learn more.

Hypertensive heart disease: a new clinical classification (VIA)

An article from the E-Journal of the ESC Council for Cardiology Practice

The working group of the Spanish Society of Cardiology proposes a clinically meaningful definition of "hypertensive cardiopathy" based on the main changes to the heart induced by chronic blood pressure elevation: alterations to the left ventricle (V), myocardial ischaemia (I), and atrial fibrillation (A). This classification encompasses the most frequent cardiac complications in patients with high blood pressure. It will improve risk stratification, and guide treatment.

Hypertension

1 - Key points

• Chronic blood pressure elevation induces a number of cardiac adaptative and detrimental changes in three main territories: left ventricle, coronary arteries, and left atrium.
• Consequently, a comprehensive definition of hypertensive heart disease should include the most important alterations documented in these three territories.
• A graded and easy-to-use classification of hypertensive heart disease, similar to the widely used TNM staging for cancer, is proposed. The acronym VIA stands for left ventricle (V), myocardial ischaemia (I), and atrial fibrillation (A).
• The VIA classification includes cardiac involvement secondary to chronic hypertension in the three main territories ranked by increasing degree of severity: V (left ventricle) (0: none; 1: hypertrophy; 2: diastolic dysfunction; 3: systolic dysfunction); I (myocardial ischaemia) (0: none; 1: microvascular ischaemia; 2: macrovascular ischaemia; 3: myocardial infarction); A (atrial fibrillation) (0: none; 1: paroxysmal; 2: permanent; 3: embolic).

2 - Background

Arterial hypertension is a highly prevalent circulatory disease1,2 that leads to severe complications if untreated3-5. Cardiac complications are the main cause of morbidity and mortality in patients with high blood pressure3,4, and also the key features influencing the choice of appropriate diagnostic procedures and of tailored antihypertensive therapy6,7.

Despite a number of studies performed over the years, no comprehensive definition and no clinically meaningful classification of hypertensive heart disease (HHD) is available. That is why the Steering Committee of the Hypertension Working Group of the Spanish Society of Cardiology developed a clinical classification of the so called “hypertensive cardiopathy” based on the three main heart components involved in patients with chronic elevated blood pressure8. This classification is briefly reviewed next.

3 - The basis for a clinical classification of hypertensive heart disease

Sustained hypertension causes structural and functional abnormalities of the heart, involving ventricular and atrial myocardium as well as epicardial and intramural coronary arteries. As a result, three different, although obviously related to each other, cardiac diseases in hypertensive patients may be recognized: heart failure, myocardial ischaemia, and atrial fibrillation9-17. These three main cardiac complications of hypertension can take place separately or combined, at different degrees of severity, or in various evolutive stages18.

Accordingly, a three-branched classification fits well for a comprehensive classification of HHD. We have adapted the most used of such a rating tool, the TNM staging classification for cancer -developed almost 50 years ago and still broadly used-, to HHD, as will be explained later. A second step has been to assign to each of the three main headings a 1-to-3 grading score (the most used in many cardiological classifications) to set cardiac complications in order, from mild or earlier to more severe or later ones.

4 - Previous definitions and classifications

The first definition of HHD was proposed in 1979 by the New York Heart Association. Hypertensive heart disease was defined as an anatomofunctional alteration characterized by left ventricular hypertrophy (LVH) and cardiac failure in patients with systemic hypertension19. With this definition, HHD was made equivalent to heart failure.

More recent definitions have also linked HHD to LVH. Frohlich et al defined HHD as the cardiac response to the afterload imposed on the left ventricle by the progressive increase in arterial pressure and peripheral vascular resistance as a consequence of hypertensive vascular disease20.

Those definitions seem incomplete. Although LVH and heart failure are the most typical cardiac complications of hypertension, many patients may however complain, especially at the beginning of the process, of other symptoms of heart involvement. At end stages arrhythmias and coronary ischaemia can also lead to a worsening of the clinical profile. The definition provided by Frohlich et al20 seems rather inadequate because, as is now well established, the hemodynamic mechanism is not the only one involved in the development of LHV21.

Several different classifications proposed for HHD (Table 1)20,22-25 have obvious drawbacks. The main one is that heart disease due to hypertension should not be restricted just to the diverse modalities of LVH. On the contrary, the classification proposed by Iriarte et al24 is somewhat original although it lacks of any reference to some usual manifestations of HHD other than heart failure, such as arrhythmias and/or myocardial ischaemia. Furthermore, the need for expensive tests to establish the diagnosis with a reasonable level of accuracy makes it difficult to put into practice this classification.

5 - The proposed classification

We propose the term hypertensive cardiopathy or hypertensive heart disease to be used to describe a complex and variable syndrome that usually, but not necessarily, includes clinical manifestations derived from: left ventricular hypertrophy and dysfunction, be it diastolic or systolic; myocardial ischemia; and rhythm abnormalities, all of them caused by the effects on the heart of chronically elevated blood pressure. Table 2 depicts the proposed comprehensive classification including those three possibilities of cardiac kinvolvement (Ventricle, Ischemia and Arrhythmia); so, the acronym VIA is proposed as well.

In terms of left ventricle involvement, the categories selected have been the three main stages of the former concept of "hypertensive heart disease": response of ventricular myocardium begins with left ventricular hypertrophy (recognised either by electrocardiography or echocardiography); afterwards, diastolic dysfunction may appear, sometimes evolving to systolic dysfunction, despite that symptoms of heart failure may be similar.

Ischaemia in hypertensive patients is frequently caused by microvascular dysfunction; if atherosclerosis develops, epicardial coronary disease and, finally, acute coronary syndromes can be present as well.

Finally, atrial fibrillation is the most common arrhythmia induced by hypertension. Despite some overlap, it usually begins in the paroxysmal form and becomes permanent later on; in some cases, an embolic event can develop as the main complication of this rhythm disturbance.

In summary, a patient with high blood pressure can be defined with this staging classification of HHD as V(0-3) I(0-3) A(0-3).

Future refinement of this classification may cover also vascular changes (cerebral, peripheral, renal) also very frequent in hypertensive patients and ususally a challenge for practitioners.

6 - Self training

Would you like to try some clinical scenarios? (answers at bottom)

1. Male patient. 65 years-old. Chronic hypertension. Transient cerebral ischaemic attack of cardioembolic origin. Echocardiogram shows EF= 65% and abnormal left ventricular filling.

2. Female patient. 83 years-old. Isolated systolic hypertension. Admitted for acute pulmonary oedema. Permanent atrial fibrillation. Echocardiogram shows EF= 38%.

3. Male patient. 57 years-old. Risk factors: heavy smoker, type 2 diabetes, and hypertension. Acute inferior myocardial infarction. Echocardiogram shows left ventricular hypertrophy, inferior akinesis, and EF= 56%.

Answers:
1. V2 I0 A3
2. V3 I0 A2
3. V1 I3 A0

Table 1: Previous classifications of hypertensive heart disease

Criteria 
: Clinical, Anatomical, Functional
Authors (year)
: WHO/ISH (1993), Framingham Study (1987),  Fröhlich (1989), Ganau et al (1992), Iriarte et al (1993)
Ref. :
22 23 20 24 25
Features : Three stages in AH according to end-organ damage, including heart (1=no; 2= signs of involvement; 3= clinical complications), Three groups according to LVH (1= dispro-portionate septal hypertrofia; 2= concen-tric LVH; 3= eccentric LVH  3a, dilated; 3b, non dilated), Four degrees according to LVH (1= no; 2=early; 3= established; 4= heart failure), Four groups according to LVH (1= normal LV; 2= concentric remodeling of LV; 3= concentric LVH; 4= eccentric LVH), Four groups according to physiopathological concepts (1= diastolic dysfunction; 2= LVH 2a, with normal FC; 2b, with impaired FC; 3= heart failure with normal EF; 4= heart failure with depressed EF)

AH: Arterial hypertension; EF: left ventricular ejection fraction; FC: functional capacity; LV: left ventricle; LVH: left ventricular hypertrophy

Table 2: The proposed "VIA" clinical classification of hypertensive heart disease

Ventricle
0: Normal
1: Left ventricular hypertroph
2: Diastolic dysfunction/failure
3: Systolic dysfunction/failure

Ischaemia
0: Not clinically manifest
1: Microvascular angina/ischaemia
2: Macrovascular angina/ischaemia
3: Myocardial infarction

Atrial fibrillation
0: None
1: Paroxysmal
2: Permanent
3. Embolic

References


1. Wolf-Maier K, Cooper RS, Banegas JR, Giampaoli S, Hense HW, Joffres M, et al. Hypertension prevalence and blood pressure levels in 6 European countries, Canada, and the United States. JAMA 2003;289:2363-9.

2. Kearney PM, Whelton M, Reynolds K, Muntner P, Whelton PK, He J. Global burden of hypertension: analysis of worldwide data. Lancet 2005;365:217-23.

3. Kannel WB. Elevated systolic blood pressure as a cardiovascular risk factor. Am J Cardiol 2000;85:251-5.

4. Turnbull F, Neal B, Ninomiya T, Algert C, Arima H, Barzi F, et al; Blood Pressure Lowering Treatment Trialists' Collaboration. Effects of different regimens to lower blood pressure on major cardiovascular events in older and younger adults: meta-analysis of randomised trials. BMJ 2008;336:1121-3.

5. Mensah GA, Croft JB, Giles WH. The heart, kidney, and brain as target organs in hypertension. Cardiol Clin 2002;20:225-47.

6. Mancia G, De Backer G, Dominiczak A, Cifkova R, Fagard R, Germano G, et al. 2007 Guidelines for the Management of Arterial Hypertension: The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). Eur Heart J 2007;28:1462-536.

7. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL, et al; Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. National Heart, Lung, and Blood Institute; National High Blood Pressure Education Program Coordinating Committee. Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003;42:1206-52.

8. Alegría E, González-Juanatey JR, González-Maqueda I. Hypertensive heart disease: A proposed clinical classification. Rev Esp Cardiol 2006;59:398-9.
9. Tin LL, Beevers DG, Lip GY. Hypertension, left ventricular hypertrophy, and sudden death. Curr Cardiol Rep 2002;4:449-57.

10. Struijker Boudier HA, Cohuet GM, Baumann M, Safar ME. The heart, macrocirculation and microcirculation in hypertension: a unifying hypothesis. J Hypertens Suppl 2003;21(Suppl 3):S19-23.
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=
11. Bhatt DL, Steg PG, Ohman EM, Hirsch AT, Ikeda Y, Mas JL, et al; the REACH Registry Investigators. International prevalence, recognition, and treatment of cardiovascular risk factors in outpatients with atherothrombosis. JAMA 2006;295:180-9.
12. De Simone G, Kitzman DW, Chinali M, Oberman A, Hopkins PN, Rao DC, et al. Left ventricular concentric geometry is associated with impaired relaxation in hypertension: the HyperGEN study. Eur Heart J 2005;26:1039-45.

13. Kostis JB. From hypertension to heart failure: update on the management of systolic and diastolic dysfunction. Am J Hypertens 2003;16(Suppl 2):18S-22S.

14. Verdecchia P, Reboldi G, Gattobigio R, Bentivoglio M, Borgioni C, Angeli F, et al. Atrial fibrillation in hypertension: predictors and outcome. Hypertension 2003;41:218-23.

15. Varela-Roman A, Grigorian L, Barge E, Bassante P, de la Peña MG, Gonzalez-Juanatey JR. Heart failure in patients with preserved and deteriorated left ventricular ejection fraction. Heart 2005;91:489-94.
16. Thomas MC, Dublin S, Kaplan RC, Glazer NL, Lumley T, Longstreth WT, et al. Blood pressure control and risk of incident atrial fibrillation. Am J Hypertens 2008;21:1111-6.

17. Verdecchia P, Angeli F, Gattobigio R, Sardone M, Porcellati C. Asymptomatic left ventricular systolic dysfunction in essential hypertension: prevalence, determinants, and prognostic value. Hypertension 2005;45:412-8.

18. Lip GYH, Felmeden DC, Li-Saw-Hee FL, Beevers DG. Hypertensive heart disease. A complex syndrome or a hypertensive "cardiomyopathy"? Eur Heart J 2000;21:1653-65.

19. The Criteria Committee of the New York Heart Association. Nomenclature and criteria for diagnosis of diseases of the heart and great vessels. Boston: Little, Brown, and Co,1979:12.
20. Frohlich ED. Evaluation and management of the patients with essential hypertension. In: Parmley WW, Chatterjee K, eds. Cardiology. Philadelphia: Lippincott,1989;23:1-15.
21. López B, Castellano JM, González A, Barba J, Díez J. Association of increased plasma cardiotrophin-1 with inappropriate left ventricular mass in essential hypertension. Hypertension 2007;50:977-83.

22. Subcommittee of WHO/ISH Mild Hypertension Liaison Committee. Summary of 1993 World Health Organisation-International Society of Hypertension: Guidelines for the management of mild hypertension. Br Med J 1993;307:1541-6.

23. Savage DD, Garrison RJ, Kannel WB, Levy D, Anderson SJ, Stokes J, et al. The spectrum of left ventricular hypertrophy in a general population sample: the Framingham study. Circulation 1987;75(Suppl 1):26-33.

24. Ganau A, Devereux RB, Roman MJ, De Simone G, Pickering TG, Saba PS, et al. Patterns of left ventricular hypertrophy and geometric remodeling in essential hypertension. J Am Coll Cardiol 1992;19:1550-8.

25. Iriarte MM, Murga N, Sagastagoitia JD, Morillas M, Boveda J, Molinero E, et al. Classification of hypertensive cardiomyopathy. Eur Heart J 1993;14(Suppl J):95-101.

VolumeNumber:

Vol7 N°20

Notes to editor


Eduardo Alegría, MD, D Phil (1)
José Ramón González-Juanatey, MD, D Phil (2)
Isidoro González-Maqueda, MD (3)

(1) Corresponding author (e-mail: ealegria@unav.es). Department of Cardiology. University Clinic of Navarra, Pamplona, Spain.
(2) Department of Cardiology. University Hospital, Santiago de Compostela, Spain.
(3) Department of Cardiology. University Hospital "La Paz", Madrid, Spain.

 

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.