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Our mission: To promote excellence in research, practice, education and policy in cardiovascular health, primary and secondary prevention.
Our goal is to reduce the burden in cardiovascular disease in Europe through percutaneous cardiovascular interventions.
Our Mission is "to improve the quality of life of the population by reducing the impact of cardiac rhythm disturbances and reduce sudden cardiac death"
To improve quality of life and logevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
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OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
Prof. Guido Grassi
Epidemiological studies convey that the obese state, particularly of the abdominal type, is a major risk factor for diabetes, coronary artery disease, myocardial infarction, heart failure, cerebrovascular disease, and sudden death. Several of these cardiovascular complications are triggered by the hypertensive state -frequently due to the obese condition. This explains why blood pressure reduction is a primary goal of therapeutic intervention, preferably making the drug choice on compounds acting on the renin-angiotensin system.
The obese state, which affects more than 20% of the adult population worldwide with prevalence trends that have steadily increased through the years, is a major risk factor for cardiovascular disease as well as for the development of hypertension.
This paper will review the pathophysiologic profile of the condition defined as “obesity-related hypertension”. It will also discuss the pharmacologic as well as the non-pharmacologic strategies to lower blood pressure values in this condition, thereby providing indications on how to effectively reduce the elevated cardiovascular risk of the obese hypertensive patients.
Epidemiological surveys performed in different countries around the world strongly support the notion that body weight, body mass index and blood pressure values are linked together by a close and direct relationship (1).
Evidence has been provided that, both in experimental animals and in humans, an increase in body fat (particularly in the abdominal area) triggers an increase in blood pressure values, which can be reversed by interventions capable of reducing body weight (2).
Over time, several hypotheses have been advanced for explaining the occurrence of a high blood pressure state in the obese population. It was initially thought that the blood pressure increase was dependent of so-called “haemodynamic factors”, i.e. on the hypervolemic state as well as on the increase in cardiac output characterising body weight gain - at least in the earlier phases of the disease (2).
As years have passed, other hypotheses have linked the development of obesity-related hypertension to metabolic, neurohumoral, renal and endothelial abnormalities.
Although we are still waiting for an “unifying theory”, some pathophysiological features have been identified as the “driving forces” of the disease (2,3). These include 1) renin-angiotensin activation, 2) stimulation of the sympathetic nervous system and 3) early occurrence of a renal dysfunction leading to glomerular hypofiltration, sodium retention as well as to microalbuminuria.
All these mechanisms may trigger a blood pressure increase via direct as well as indirect mechanisms. This being the case because 1) angiotensin II increases peripheral vascular resistance and exerts powerful central pressor effects, 2) adrenergic drive promotes peripheral and renal vasoconstriction and, trough these mechanisms, elicits sodium retention and 3) renal impairment favours an elevation in blood pressure levels (2-3). Other pathophysiological mechanisms, however, participate in the phenomenon. These include, for example, the insulin resistance state (and the related hyperinsulinemia) which is common in obesity and exerts sympathostimulatory and vasoconstrictive effects (4). They also include the increase in circulating levels of leptin, i.e. the adipocyte-derived hormone which may display pressor and sympathoexcitatory effects (5). A further mechanism is represented with the high prevalence in the obese state of the sleep apnea syndrome which, via a chemoreflex dysfunction, may further potentiate the already elevated adrenergic cardiovascular drive (3).
Non pharmacological interventions aimed at lowering body weight, such as dietary restrictions in caloric intake and/or measures to improve physical fitness, have been shown to 1) decrease blood pressure, 2) favorably modify the obesity-related increase in metabolic risk factors and 3) improve, or even restore to normal the metabolic, sympathetic, neurohumoral and endothelial dysfunctions (6).
However, long term maintenance of a reduced body weight is a difficult goal to achieve, making it necessary to base treatment strategies on correction of cardiovascular risk factors, including the hypertensive state.
Which blood pressure lowering strategy should be indicated in obesity-related hypertension remains a matter of debate (7) for the following reasons: 1) there are currently no therapeutic recommendations for the disease and 2) there are very few investigations specifically addressing this issue in obese populations.
From the results of two of them - the Treatment in Obese Patients with Hypertension (TROPHY, 8) and the Candesartan Role on Obesity and Sympathetic System (CROSS, 9) study - the following conclusions can be drawn:
Finally, two further issues should be briefly mentioned. First, central sympatholitic agents may exert favourable metabolic effects by improving insulin sensitivity and ameliorating lipid profile (12). Second, although confined to patients affected with metabolic syndrome, the suggestion has recently been made that goal blood pressure values during antihypertensive treatment should be well below 140/90 mmHg (possibly below 130/80 mmHg in patients with diabetes) (13).
This means that combination therapy is in most instances mandatory to reduce blood pressure values at goal and thus to achieve full cardiovascular protection.
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.
1. Haffner S, Taegtmeyer H. Epidemic obesity and metabolic syndrome. Circulation 2003;108:1541-1545. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14517149&query_hl=1&itool=pubmed_docsum 2. Hall JE. The kidney, hypertension and obesity. Hypertension 2003;41:625-633. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12623970&query_hl=3&itool=pubmed_docsum 3. Grassi G, Seravalle G, Quarti Trevano F, et al. Effects of hypertension and obesity on the sympathetic activation of heart failure patients. Hypertension 2003;42:873-877. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14568999&query_hl=7&itool=pubmed_docsum 4. Ginsber G. Insulin resistance and cardiovascular disease. J Clin Invest 2000;106:453-458. 5. Mark AL, Correia M, Morgan DA, et al. State-of-the-art-lecture: Obesity-induced hypertension: new concepts from the emerging biology of obesity. Hypertension 1999;33:537-541. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9931161&query_hl=27&itool=pubmed_docsum 6. Miller ER, Erlinger TP, Young DR, et al. Results of the Diet, Exercise and Weight Loss Intervention Trial (DEW-IT). Hypertension 2002;40:612-618. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12411452&query_hl=11&itool=pubmed_docsum 7. Sharma AM, Pischon T, Engeli S, et al. Choice of drug treatment for obesity-related hypertension: where is the evidence? J Hypertens 2001;19:667-674. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11330867&query_hl=14&itool=pubmed_docsum 8. Reisin E, Weir MR, Falkner B, et al. for the Treatment in Obese Patients with Hypertension (TROPHY) Study Group. Lisinopril versus hydrochlorothiazide in obese hypertensive patients: a multicenter placebo-controlled trial. Hypertens 1997;30:140-145. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9231834&query_hl=16&itool=pubmed_docsum 9. Grassi G, Seravalle G, Dell’Oro R, et al. Comparative effects of candesartan and hydrocholorothiazide on blood pressare, insulin sensitivity and sympathetic drive in obese hypertensive individuals: results of the CROSS study. J Hypertens 2003;21:1761-1769. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12923410&query_hl=7&itool=pubmed_docsum 10. Mancia G, Grassi G, Zanchetti A. new-onset diabetes and antihypertensive drugs. J Hypertens 2006;24:3-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16331092&query_hl=19&itool=pubmed_docsum 11. Sharma AM, Pischon T, Hardt S, et al. ?-adrenergic receptor blockers and weight gain: a systematic analysis. Hypertension 2001;37:250-254. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11230280&query_hl=21&itool=pubmed_docsum 12. Haenni A, Lithell H. Monoxidine improves insulin sensitivity in insulin-resistant hypertensives. J Hypertens 1999;17(Suppl.):S29-S35. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10489096&query_hl=23&itool=pubmed_docsum 13. Grundy SM, Cleeman JI, Daniels SR, et al. Diagnosis and management of the metabolic syndrome. An AHA/NHLBI Scientific statement. Circulation 2005;112:2735-2752. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16157765&query_hl=25&itool=pubmed_docsum
Prof G. Grassi Monza, Italy Chairman of the Working Group on Hypertension and the Heart