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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2001-4-17
pubmed:abstractText
In hypertension, both reduced vascular supply and increased cardiac demand contribute to the development of (silent) myocardial ischemia. Our aim was to determine the prevalence of ST-segment depression and to analyze contributing factors in asymptomatic, previously untreated, older hypertensives. From a population survey, in 184 patients with mild hypertension (4 times systolic blood pressure >/=160 mm Hg and/or diastolic blood pressure >/=95 mm Hg), 60 to 75 years of age, cardiovascular end-organ damage was measured. Episodes of ST-segment depression were measured by 48-hour ambulatory Holter monitoring and were observed in 21 hypertensives (12%). They showed a significantly higher combined far-wall intima-media thickness of carotid and femoral arteries and more arterial plaques as measured by B-mode ultrasound compared with hypertensives without ST depression (0.00098+/-0.00021 versus 0.00088+/-0.00016 mm and 5.2+/-3.7 versus 3.7+/-2.8 plaques, P<0.05, respectively), whereas left ventricular mass index was not different (111+/-18 versus 104+/-24 g/m(2); P=0.18, respectively). In hypertensives with transient ST-segment depression, a significant relation was found between left ventricular mass and ischemic burden (r=0.51, P=0.02). Approximately 1 of 8 unselected and previously untreated older hypertensives show asymptomatic ST-segment depression, suggestive of silent myocardial ischemia. These data suggest that vascular factors mainly determine the occurrence of ischemic ST-segment depression and cardiac factors determine the ischemic burden in older hypertensives.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1524-4563
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
37
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1083-8
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Silent ST depression and cardiovascular end-organ damage in newly found, older hypertensives.
pubmed:affiliation
Department of Cardiology/Thoraxcenter, University Hospital Groningen, The Netherlands. w.f.terpstra@castel.nl.
pubmed:publicationType
Journal Article