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Hypertension and Coronary Heart Disease Journal of Human Hypertension (2002) 16 (Suppl 1), S61–S63 2002 Nature Publishing Group All rights reserved 0950-9240/02 $25.00 www.nature.com/jhh Hypertension and coronary heart disease E Escobar University of Chile, Santiago, Chile The association of hypertension and coronary heart atherosclerosis, damage of arterial territories other than disease is a frequent one. There are several patho- the coronary one, and of the extension and severity of physiologic mechanisms which link both diseases. coronary artery involvement. It is important to empha- Hypertension induces endothelial dysfunction, exacer- sise that complications and mortality of patients suffer- bates the atherosclerotic process and it contributes to ing a myocardial infarction are greater in hypertensive make the atherosclerotic plaque more unstable. Left patients. Treatment should be aimed to achieve optimal ventricular hypertrophy, which is the usual complication values of blood pressure, and all the strategies to treat of hypertension, promotes a decrease of ‘coronary coronary heart disease should be considered on an indi- reserve’ and increases myocardial oxygen demand, vidual basis. both mechanisms contributing to myocardial ischaemia. Journal of Human Hypertension (2002) 16 (Suppl 1), S61– From a clinical point of view hypertensive patients S63. DOI: 10.1038/sj/jhh/1001345 should have a complete evaluation of risk factors for Keywords: hypertension; hypertrophy; coronary heart disease There is a strong and frequent association between arterial hypertension.8 Hypertension is frequently arterial hypertension and coronary heart disease associated to metabolic disorders, such as insulin (CHD). In the PROCAM study, in men between 40 resistance with hyperinsulinaemia and dyslipidae- and 66 years of age, the prevalence of hypertension mia, which are additional risk factors of atheroscler- in patients who had a myocardial infarction was osis.9 14/1000 men in a follow-up of 4 years. This figure Deposition of lipids and the formation of the increased to 48 when hypertension was associated atherosclerotic plaque may be favoured by the to diabetes mellitus and 114 when it was associated increase of transmural pressure in arterial vessels, to diabetes and hyperlipidaemia.1 Major secondary with an increase in mechanical stress and endo- prevention trials with statins (4S, CARE and LIPID), thelial permeability. Furthermore, it is well docu- included patients with myocardial infarction and mented that there is endothelial dysfunction, angina pectoris. If baseline characteristics of these remodelling of coronary arteries and increased trials are analysed it is observed that patients in the resistance at microvascular level, all contributing to 4S study had hypertension in 26% of the cases,2 and a decrease of coronary reserve.10 patients in the CARE3 and LIPID4 studies had 43% Coronary reserve is impaired in patients with and 41% incidence of hypertension respectively. On essential arterial hypertension in the absence of the other hand the mortality rate of CHD is 2.3 times CHD,10 which is explained in part by the presence greater when hypertension is present.5 of left ventricular hypertrophy. Experimental stud- There is no doubt that the magnitude of hyperten- ies have shown that minimal coronary resistance is sion does have an impact in the incidence of CHD. increased in spontaneous hypertensive rats, along If the risk ratio is 1 for a diastolic pressure Ͻ80 with a decrease in capillary density and coronary mm Hg, this ratio increases progressively when dia- reserve.11 stolic pressure is higher, and at least duplicates at In dogs with chronic renovascular hypertension values of 94 mm Hg or more.6 and left ventricular hypertrophy it has been shown Risk ratio for myocardial infarction is 1 when sys- that the wall/lumen ratio is not significantly tolic pressure is between 120 and 129 mm Hg, and increased in arterioles and arteries of different sizes, almost 2 when this value is greater than 140 compared with normotensive animals. An increase mm Hg.7 There are important pathophysiologic links in the wall/lumen ratio would not explain the between arterial hypertension and CHD which increased vascular resistance.12 This increased might explain the pathogenenesis of CHD when resistance has been confirmed in patients; flow is hypertension is present. also increased along with a significant increase of First of all, atherosclerosis is exacerbated by myocardial oxygen consumption.13 It has been recently confirmed that coronary blood flow is increased in hypertensive patients with left Correspondence: E Escobar, Av. Salvador 465, Santiago, Chile ventricular hypertrophy compared with hyperten- sives without hypertrophy and normotensives. Hypertension and coronary heart disease E Escobar S62 The lumen area was similar in hypertensives with decreased coronary reserve, clinical manifestations hypertrophy of the left ventricle and normotensives, of CHD (angina, myocardial infarction) are frequent and significantly greater than hypertensives without in hypertensive patients. Resting electrocardiogram hypertrophy. Vessel area was significantly greater in show alterations of repolarisation suggestive of hypertensives with hypertrophy than in those with- ischaemia and exercise tests may have a false- out. Vessel area increased significantly with plaque positive response. Ischaemia may also contribute to area in the three groups. On the other hand produce subendocardial fibrosis which in turn con- responses to acetilcholine (endothelium dependent) tribute to diastolic as well as to systolic dysfunction. and to adenosine (non-endothelial dependent) are It has been suggested that acute coronary syn- significantly decreased in patients with left ven- dromes might be favoured by an increased flow velo- tricular hypertrophy.14 city and shear stress which could contribute to These results suggest that functional abnormali- plaque disruption. It has been shown in hyperten- ties in humans with hypertension and left ventricu- sive patients with normal coronary arteries that flow lar hypertrophy are associated with structural velocity is increased which is only partially changes, namely coronary remodelling. reversed by isosorbide.21 The increase in lumen area would contribute to In hypertensives with left ventricular hypertrophy maintain a constant flow velocity in large epicardial the risk of reinfarction, overall mortality and mor- arteries and as a consequence a normal endothelial tality due to CHD are significantly increased.22 function with a normal shear stress. This would It is important to emphasise that treatment of result in a reduced release of endothelium-derived hypertension reduces significantly the number of relaxing factor which is known to be a potent vaso- fatal and non-fatal cardiovascular events in patients dilator, inhibits proliferation of vascular smooth with CHD.23,24 muscle cells, endothelial movement and extracellu- General principles for the treatment of hyperten- lar matrix production.14 sion fully apply to patients with hypertension and In an experimental model in rats, coronary CHD. Recent data from the Hypertension Optimal hypertension (banding of ascending aorta) without Treatment (HOT) Trial in a cohort of 19000 patients, hypertrophy (right ventricle) remodelling was show no evidence of increased mortality when dias- expressed in arterial microvessels larger than 30 ␮m tolic blood pressure fell below 85 mm Hg, contra- but not in small microvesels (30 ␮m). Medial thick- dicting former data of an increased mortality when ening by proliferation of smooth muscle cells and treated diastolic blood pressure fell below that figure perivascular fibrosis were observed.15 (J curve).25 It is advisable to avoid sudden decreases On the other hand, in myocardial hypertrophy in blood pressure values and tachycardia when without coronary hypertension (pulmonary artery angina pectoris is present. Vasodilator agents may banding) no vascular hypertrophy was observed, but cause reflex stimulation of baroreceptors and tachy- deposition of collagen in perivascular tissues of cardia and increased contractility resulting in small microvesels (Ͻ60 ␮m in lumen diameter).15 increased myocardial oxygen demand and thus Cardiac renin-angiotensin-aldosterone system, endo- aggravating angina. On that respect, hydralazine or thelial growth factor, platelet derived growth factors, short-acting calcium antagonists should be avoided. atrial natriuretic peptide, and endothelin among Global evaluation of the patient is mandatory. It other susbstances may be involved in this is important to evaluate the extension of organic response.16 Increased wall stress owing to pressure damage, the presence of diabetes and other risk fac- overload may stimulate perivascular fibroblasts pro- tors, and the presence of aggravating factors such as liferation and extracellular matrix proteins by thyrotoxicosis and anaemia, etc, and obviously the these cells. severity and extension of coronary disease. Non- When coronary hypertension is combined with pharmacologic and pharmacologic treatment must hypertrophy, as is often the case in systemic arterial be linked to reduce overall cardiovascular risk. hypertension, the two remodelling processes Furthermore stabilisation of atherosclerotic described are superimposed.17 Medial hypertrophy plaque is of extreme importance. Antithrombotic and perivascular collagen deposition have been agents, as well as statins when necessary, are observed in small and larger microvessels in a study important on
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