Hypertension and stable coronary artery disease

Abstract

Systemic hypertension is highly prevalent in stable coronary artery disease, a pervasive comorbidity complicating the diagnostic performance and interpretation of non-invasive provocative tests in chest pain patients because of the ischaemic signals generated, despite normal or near normal coronary arteries, by hearts structurally readapted by long-term exposure to raised systemic blood pressure. Additional and unresolved problems posed by arterial hypertension in patients with stable coronary artery disease regard the benefits of antihypertensive treatment due to reports of irrelevant, if not detrimental, effect of blood pressure (BP) lowering in averting coronary relapses as well as the lack of association between BP levels and incident coronary events in survivors from acute myocardial infarction. Uncertainties extend to BP-independent cardioprotective effects of antihypertensive drugs, although the efficacy of renin-angiotensin system blockers in the long-term prevention of cardiovascular events in stable coronary artery disease patients has been shown by several studies, particularly when combined with amlodipine, a dihydropiridine calcium channel blocker. In contrast, the long-term effect of beta-blockers, the antihypertensive class most used in that clinical category, is not supported by strong evidence except that generated in patients with systolic dysfunction and early postmyocardial infarction recovery periods.

Ventricular–vascular coupling in hypertension

“…125,126 The early return of reflected waves to central arterial districts can therefore be figured as a poorly timed intra-aortic balloon pump, which increases left ventricular afterload and myocardial oxygen consumption while simultaneously reducing diastolic pressure in ascending aorta and, as a consequence, coronary perfusion. 13 The clinical impact of pressure wave reflection is not limited to left ventricular load and coronary perfusion.…”

Human AGT -p.Met268Thr and coronary heart disease risk: a case-control study and meta-analysis

“…Polymorphism in some key genes, such as nitric oxide synthase (OMIM: 600720) [36] and p22phox (OMIM: 608508) [51], might be genetic risk factors for cardiovascular disease. Genes involved in the renin-angiotensin system, such as angiotensinogen [11], angiotensin I-converting enzyme [12] and angiotensin ii type 1 receptor [13], are good candidates to study CHd genetic risk factors. This system is well known to be involved in the control of blood pressure and plays an autocrine or paracrine role in cardiac remodeling and contributes to the pathophysiology of CHD [52,53].…”

“…in humans, the rennin-angiotensin system (ras) plays an important role in the maintenance of salt-water balance and controlling blood pressure [9,10]. Several genes are participating in ras pathways as angiotensinogen (AGT; OMIM: 106150) [11], angiotensin I-converting enzyme (ACE; OMIM: 106180) [12] and angiotensin II type 1 receptor (AGTR1; OMIM: 106165) [13], which are noteworthy targets. these genes are considered to influence the inherited predisposition toward CHD [14].…”

New Methods of Assessment of Subclinical Changes in the Cardiovascular System in Arterial Hypertension

“…Изменение условий нагрузки из-за раннего от-ражения волн увеличивает потребление кислорода миокардом, в то время как сопутствующее снижение диастолического АД снижает коронарную перфузию [37]. Эта неблагоприятная комбинация способствует ишемии миокарда [38]. Раннее возвращение отраженных волн в центральные артерии может быть расценено как диссинхронизация работы внутриаортальной баллон-ной помпы, которая приводит к увеличению постна-грузки на ЛЖ и потребности миокарда в кислороде, од-новременно приводя к снижению диастолического АД в восходящей аорте и, как следствие, перфузии мио-карда.…”

“…Пациенты с АГ и высоким эффективным артери-альным эластансом имеют почти в три раза большую (30 против 9%) распространенность концентрического ремоделирования миокарда ЛЖ, чем пациенты с АГ и нормальным артериальным эластансом [26] Повы-шение эффективного артериального эластанса связа-но не только с относительно небольшим размером по-лости ЛЖ, но и с большей относительной толщиной стен-ки в общей популяции [38]. Необходимы дальнейшие исследования в более широких группах наблюдения, чтобы подтвердить эти данные.…”