Microvascular angina pectoris in hypertensive patients with left ventricular hypertrophy and diagnostic value of exercise Thallium-201 scintigraphy

Iriarte, Marian; Caso, Rosario; Murga, Nekane; Faus, J. M.; Sagastagoitia, D; Molinero, E; Argumedo, Marta Lo ́pez de; Bòveda, J

doi:10.1016/s0002-9149(99)80549-9

Cited by 57 publications

(19 citation statements)

References 18 publications

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“…[52][53][54] These changes have been associated clinically with interstitial ventricular fibrosis and myocardial infarction in the absence of atherosclerotic occlusive epicardial disease, 61 as found in our model of SHR treated with L-NAME.…”

Section: Discussionsupporting

confidence: 65%

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Apoptosis, Coronary Arterial Remodeling, and Myocardial Infarction After Nitric Oxide Inhibition in SHR

Ono

Matsuoka

et al. 1999

Hypertension

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Abstract-This study was designed to investigate the relationship between apoptosis (programmed cell death) and coronary arterial remodeling in spontaneously hypertensive rats (SHR) following prolonged nitric oxide synthesis inhibition. In addition, we evaluated whether the development of coronary arterial smooth muscular cell apoptosis was related to hemodynamics or to vascular hypertrophy. Three groups of 20-week-old male SHR were investigated: controls, and two groups that received two doses of N G -nitro-L arginine (L-NAME, 50 mg/L and 80 mg/L) each for 3 weeks. Mean arterial pressure and total peripheral resistance index increased whereas cardiac index diminished with L-NAME. Pathohistological study demonstrated increased pericardiac fibrosis and coronary arterial injury score in the L-NAME group in a dose-dependent manner. The high dose of L-NAME (Group 3) produced myocardial infarction in 78% of the rats. The wall:lumen ratio of epicardial coronary arteries was greater in L-NAME treated SHR (0.23Ϯ0.02 versus 0.16Ϯ0.02; PϽ0.05) and was associated with markedly increased apoptosis (15.3Ϯ6 versus 1.9Ϯ1; PϽ0.05) without smooth muscle cell proliferation (PCNA positive cells). Apoptosis occurred predominantly in hypertrophic coronary arterial smooth muscular cells; myocardial infarction and ventricular fibrosis were exacerbated by impaired hemodynamics induced by L-NAME. These data suggest that coronary endothelial dysfunction and myocardial ischemic disease induced by L-NAME were responsible for apoptosis of coronary arterial smooth muscle cells, myocardial fibrosis, and infarction, all pathological findings that are consistent with what may be found in clinical hypertensive heart disease. (Hypertension. 1999;34:609-616.)

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Section: Discussionsupporting

confidence: 65%

“…[52][53][54] Moreover, in this study, the wall:lumen ratio of L-NAMEtreated SHR was increased in a dose-dependent manner. Deng et al 55,56 have evaluated, in similar L-NAME-treated SHR, the prepro-endothelin (ET)-1 mRNA expression using in situ hybridization methods.…”

Section: Discussionsupporting

confidence: 62%

Apoptosis, Coronary Arterial Remodeling, and Myocardial Infarction After Nitric Oxide Inhibition in SHR

Ono

Matsuoka

et al. 1999

Hypertension

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“…perfusion defects can be attributed to impaired coronary flow reserve, especially when LVH coexists [13,14]. Furthermore, Iriarte et al have reported that the majority (62%) of hypertensive patients with LVH and angina pectoris present with normal epicardial coronary arteries, while angina-like symptoms could be attributed to smallvessel disease [15]. Thus, one could say that the characterization as "false-positive" for SPECT results in hypertensive patients with angina-like syndrome and normal epicardial coronary arteries may not be successful, since most of these patients seem to present microvascular type of myocardial ischemia.…”

Section: Discussionmentioning

confidence: 99%

Hypertensive patients with false-positive Thallium-201 scintigraphic results in the infero-posterior wall are in high risk for coronary artery disease development

Michaelides¹,

Tousoulis²,

Fourlas³

et al. 2007

International Journal of Cardiology

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“…The phenomenon of reduced perfusion secondary to microvascular disease in this setting has been previously recognised and probably explains the ischaemic symptoms experienced by some hypertensive patients with normal coronary arteries. 24,25 The access of diagnostic tests to the treating clinician will clearly influence practice. Most clinicians treating hypertension would recognise the importance of an ECG at initial assessment and it is now clear that echocardiographic assessment for LVH imparts additional important information.…”

Section: Discussionmentioning

confidence: 99%

The accuracy of non-invasive methods for the detection of obstructive coronary artery disease in the presence of left ventricular hypertrophy

Hogg

Metcalfe

2000

J Hum Hypertens

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Microvascular angina pectoris in hypertensive patients with left ventricular hypertrophy and diagnostic value of exercise Thallium-201 scintigraphy

Cited by 57 publications

References 18 publications

Apoptosis, Coronary Arterial Remodeling, and Myocardial Infarction After Nitric Oxide Inhibition in SHR

Apoptosis, Coronary Arterial Remodeling, and Myocardial Infarction After Nitric Oxide Inhibition in SHR

Hypertensive patients with false-positive Thallium-201 scintigraphic results in the infero-posterior wall are in high risk for coronary artery disease development

The accuracy of non-invasive methods for the detection of obstructive coronary artery disease in the presence of left ventricular hypertrophy

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