Structural and functional alterations of the intramyocardial coronary arterioles in patients with arterial hypertension.

Schwartzkopff, B.; Motz, W.; Frenzel, H; Vogt, M.; Knauer, Sabine; Strauer, B. E.

doi:10.1161/01.cir.88.3.993

Cited by 357 publications

(203 citation statements)

References 44 publications

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“…4 Several factors are involved in reducing CFR in hypertensive patients, such as higher BP per se, increased LV mass and endsystolic stress, or a reduction in the overall maximal cross-sectional area of the microcirculatory bed due to increased coronary arteriolar tone, endothelial dysfunction, inadequate angiogenesis or extravascular compression. 2,3,[22][23][24] In the present study, lower values of CFR in hypertensive patients were accompanied by greater LV mass, lower transmitral E/A and myocardial Em/Am ratio, as well as reduced SEVR. Moreover, SEVR and myocardial Em/Am ratio, along with LV mass index, were associated with CFR independently from other clinical and echocardiographic variables.…”

Section: Coronary Flow Reserve and Buckberg Index D Tsiachris Et Alsupporting

confidence: 62%

Subendocardial viability ratio as an index of impaired coronary flow reserve in hypertensives without significant coronary artery stenoses

et al. 2011

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Subendocardial viability ratio (SEVR), calculated through pulse wave analysis, is an index of myocardial oxygen supply and demand. Our aim was to evaluate the relationship between coronary flow reserve (CFR) and SEVR in 36 consecutive untreated hypertensives (aged 57.9 years, 12 males, all Caucasian) with indications of myocardial ischaemia and normal coronary arteries in coronary angiography. CFR was calculated by a 0.014-inch Doppler guidewire (Flowire, Volcano, San Diego, CA, USA) in response to bolus intracoronary administration of adenosine (30-60 lg). SEVR was calculated by radial applanation tonometry, while diastolic function was evaluated by means of transmitral flow and tissue Doppler imaging. Hypertensive patients with low CFR (n ¼ 24) compared with those with normal CFR (n ¼ 12) exhibited significantly decreased SEVR by 24.5% (P ¼ 0.002). In hypertensives with low CFR, CFR was correlated with SEVR (r ¼ 0.651, P ¼ 0.001). After applying multivariate linear regression analysis, age, left ventricular mass index, Em/Am, 24-h diastolic blood pressure (BP) and SEVR turned out to be the only independent predictors of CFR (adjusted R 2 ¼ 0.718). Estimation of SEVR by using applanation tonometry may provide a reliable tool for the assessment of coronary microcirculation in essential hypertensives with indications of myocardial ischaemia and normal coronary arteries.

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Section: Coronary Flow Reserve and Buckberg Index D Tsiachris Et Alsupporting

confidence: 62%

Subendocardial viability ratio as an index of impaired coronary flow reserve in hypertensives without significant coronary artery stenoses

et al. 2011

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“…Lower myocardial contractility may be associated with lower coronary blood flow; however, the association of lower resting myocardial contractility to lower CFR by dipyridamole stress testing is new. Since impaired myocardial contractility is associated with higher myocardial fibrosis, and structural remodelling of the intramyocardial coronary arterioles and the accumulation of fibrillar collagen are decisive factors for a reduced coronary dilatory capacity, 36 our findings may suggest that impaired myocardial contractility may characterize a cardiac phenotype associated with initial impairment of CFR already in the early stage of uncomplicated arterial hypertension, and independent to coronary artery stenosis.…”

Section: Discussionmentioning

confidence: 66%

Relations of left ventricular mass and systolic function to endothelial function and coronary flow reserve in healthy, new discovered hypertensive subjects

et al. 2005

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Left ventricular hypertrophy (LVH) is prognostically relevant, associated with major cardiovascular risk factors and with atherosclerosis. However, whether LVH is independently associated with impaired coronary flow reserve (CFR) and with endothelial dysfunction is disputed. We assessed the relationship of LV mass and systolic function to CFR and endothelial function in new discovered never treated subjects with essential arterial hypertension, but without coronary artery disease or microalbuminuria. LVH, ejection fraction (EF) and stress-corrected midwall shortening (MWS, a measure of myocardial contractility) were assessed by echocardiography. CFR was assessed by single-photon emission computed tomography and dipyridamole infusion. Endothelial function was evaluated by assessing 1-min postischaemic flow-mediated dilatation of the brachial artery (FMD); nitroglycerine-mediated dilatation (NMD) of the same brachial artery was used as measure of nonendothelium-dependent vasodilatation. In approximately 1 year, we enrolled 21 subjects who met stringent inclusion criteria (47710 years old, 26.672.8 kg/m 2 , 78% men). Five patients showed LVH. Multivariate analyses showed a significant negative correlation of LV mass index with FMD (b ¼ À0.61, Po0.05) but not with NMD, neither with CFR. Stress-corrected MWS showed independent correlation with CFR (b ¼ 0.51, Po0.05). Thus, in clinically healthy, new discovered hypertensive subjects, never treated and mostly in the early stage of arterial hypertension, LVH can be associated with endothelial dysfunction while maximal dipyridamoledependent CFR may be preserved; nevertheless, a cardiac phenotype presenting with tendency to impaired myocardial contractility, assessed by stress-corrected MWS, showed association with lower CFR in the early stage of arterial hypertension.

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“…17 Medial hypertrophy and perivascular collagen deposition have been observed in small and larger microvessels in a study in humans by biopsy samples 18 and in autopsies of hypertensive patients. 19 Experimental data show that after relief of pressure overload there is a regression of medial hypertrophy and perivascular collagen, first at larger arterial microvessels and then in small microvessels 17 but perivascular collagen deposition may remain.…”

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confidence: 99%

Hypertension and coronary heart disease

Escobar

2002

J Hum Hypertens

115

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The association of hypertension and coronary heart disease is a frequent one. There are several pathophysiologic mechanisms which link both diseases. Hypertension induces endothelial dysfunction, exacerbates the atherosclerotic process and it contributes to make the atherosclerotic plaque more unstable. Left ventricular hypertrophy, which is the usual complication of hypertension, promotes a decrease of 'coronary reserve' and increases myocardial oxygen demand, both mechanisms contributing to myocardial ischaemia. From a clinical point of view hypertensive patients 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 and coronary heart disease (CHD). In the PROCAM study, in men between 40 and 66 years of age, the prevalence of hypertension in patients who had a myocardial infarction was 14/1000 men in a follow-up of 4 years. This figure increased to 48 when hypertension was associated to diabetes mellitus and 114 when it was associated to diabetes and hyperlipidaemia. 1 Major secondary prevention trials with statins (4S, CARE and LIPID), included patients with myocardial infarction and angina pectoris. If baseline characteristics of these trials are analysed it is observed that patients in the 4S study had hypertension in 26% of the cases, 2 and patients in the CARE 3 and LIPID 4 studies had 43% and 41% incidence of hypertension respectively. On the other hand the mortality rate of CHD is 2.3 times greater when hypertension is present. 5 There is no doubt that the magnitude of hypertension does have an impact in the incidence of CHD. If the risk ratio is 1 for a diastolic pressure Ͻ80 mm Hg, this ratio increases progressively when diastolic pressure is higher, and at least duplicates at values of 94 mm Hg or more. 6 Risk ratio for myocardial infarction is 1 when systolic pressure is between 120 and 129 mm Hg, and almost 2 when this value is greater than 140 mm Hg. 7 There are important pathophysiologic links between arterial hypertension and CHD which might explain the pathogenenesis of CHD when hypertension is present.First of all, atherosclerosis is exacerbated by arterial hypertension. 8 Hypertension is frequently associated to metabolic disorders, such as insulin resistance with hyperinsulinaemia and dyslipidaemia, which are additional risk factors of atherosclerosis. 9 Deposition of lipids and the formation of the atherosclerotic plaque may be favoured by the increase of transmural pressure in arterial vessels, with an increase in mechanical stress and endothelial permeability. Furthermore, it is well documented that there is endothelial dysfunction, remodelling of coronary arteries and increased resistance at microvascular level, all contributing to a decrease of coronary reserve. 10 Coronary reserve is impaired in patients with essential arterial hypertension in the absence of CHD, 10 which is explained in part by the presence of left ventricular hypertrophy. Experimental s...

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Structural and functional alterations of the intramyocardial coronary arterioles in patients with arterial hypertension.

Abstract: Structural remodeling of the intramyocardial coronary arterioles and the accumulation of fibrillar collagen are decisive factors for a reduced coronary dilatory capacity in patients with arterial hypertension and angina pectoris in the absence of relevant coronary artery stenoses.

Cited by 357 publications

References 44 publications

Subendocardial viability ratio as an index of impaired coronary flow reserve in hypertensives without significant coronary artery stenoses

Subendocardial viability ratio as an index of impaired coronary flow reserve in hypertensives without significant coronary artery stenoses

Relations of left ventricular mass and systolic function to endothelial function and coronary flow reserve in healthy, new discovered hypertensive subjects

Hypertension and coronary heart disease

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