{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,10]],"date-time":"2026-08-10T10:42:31Z","timestamp":1786358551440,"version":"build-2736575974"},"reference-count":0,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[1992,6]]},"abstract":"<jats:sec>\n            <jats:title>BACKGROUND<\/jats:title>\n            <jats:p>Syncope and sudden death in hypertrophic cardiomyopathy may have a hemodynamic basis. The presence of a small ventricular cavity with high intracavity pressures may activate left ventricular baroreceptors and cause reflex hypotension as described in other populations with syncope.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>METHODS AND RESULTS<\/jats:title>\n            <jats:p>To investigate this potential mechanism of syncope in hypertrophic cardiomyopathy, we studied 17 patients with a history of syncope (syncopal), 19 without syncope (nonsyncopal), and nine normal control subjects by using a head-up tilt test. Head-up tilt at 60 degrees for 45 minutes was followed by 10-minute tilts during incremental doses of isoprenaline. Heart rate, blood pressure, and two-dimensional and Doppler echocardiography were monitored throughout. On tilting, hypertrophic cardiomyopathy patients showed a decline in mean arterial pressure of -5 +\/- 6 mm Hg (p less than 0.001) compared with no change in control subjects (0.2 +\/- 6 mm Hg, p = 0.9). Left ventricular outflow tract velocity decreased on tilting in control subjects (-8 +\/- 6 cm\/sec, p = 0.004) but increased in the syncopal and nonsyncopal patients (20 +\/- 50 cm\/sec, p = 0.05). Reflex hypotension with or without bradycardia, associated with syncope or presyncope, was induced in seven syncopal patients, two nonsyncopal patients, and two control subjects (p = 0.05). The early response to tilt in these subjects was characterized by maintenance of blood pressure but a greater increase in left ventricular fractional shortening than in the other subjects (10 +\/- 8% versus 1 +\/- 1%, p = 0.002). The onset of hypotension was associated with a trend toward further decreases in left ventricular diameters, outflow tract velocity, and transmitral flow velocities. In the remaining patients who had a negative test, transient hypotension (systolic pressure less than 100 mm Hg) occurred in seven syncopal patients and three nonsyncopal patients compared with none of the control subjects (p = 0.01). In total, hypotension was demonstrated in 82% of syncopal patients compared with 26% of nonsyncopal patients and 22% of control subjects (p = 0.001).<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>CONCLUSIONS<\/jats:title>\n            <jats:p>Patients with hypertrophic cardiomyopathy and a history of syncope frequently display hypotension during head-up tilt. In some cases, sudden hypotension occurs and is usually associated with bradycardia and a reduced cavity size, findings compatible with activation of a ventricular baroreflex. In other cases, transient hypotension occurs and could be explained by an impairment of baroreceptor function. These mechanisms may contribute to the occurrence of syncope in daily life.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/01.cir.85.6.2140","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:01:09Z","timestamp":1339459269000},"page":"2140-2148","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":45,"title":["Investigation of a hemodynamic basis for syncope in hypertrophic cardiomyopathy. Use of a head-up tilt test."],"prefix":"10.1161","volume":"85","author":[{"given":"D M","family":"Gilligan","sequence":"first","affiliation":[{"name":"Department of Medicine (Clinical Cardiology), Royal Postgraduate Medical School, Hammersmith Hospital, London."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P","family":"Nihoyannopoulos","sequence":"additional","affiliation":[{"name":"Department of Medicine (Clinical Cardiology), Royal Postgraduate Medical School, Hammersmith Hospital, London."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"W L","family":"Chan","sequence":"additional","affiliation":[{"name":"Department of Medicine (Clinical Cardiology), Royal Postgraduate Medical School, Hammersmith Hospital, London."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C M","family":"Oakley","sequence":"additional","affiliation":[{"name":"Department of Medicine (Clinical Cardiology), Royal Postgraduate Medical School, Hammersmith Hospital, London."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","container-title":["Circulation"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.ahajournals.org\/doi\/pdf\/10.1161\/01.CIR.85.6.2140","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T16:05:33Z","timestamp":1715529933000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.ahajournals.org\/doi\/10.1161\/01.CIR.85.6.2140"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1992,6]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1992,6]]}},"alternative-id":["10.1161\/01.CIR.85.6.2140"],"URL":"https:\/\/doi.org\/10.1161\/01.cir.85.6.2140","relation":{},"ISSN":["0009-7322","1524-4539"],"issn-type":[{"value":"0009-7322","type":"print"},{"value":"1524-4539","type":"electronic"}],"subject":[],"published":{"date-parts":[[1992,6]]},"assertion":[{"value":"1992-06-01","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}