Pericardial pressure in experimental chronic heart failure

Citation
Sg. Horne et al., Pericardial pressure in experimental chronic heart failure, CAN J CARD, 16(5), 2000, pp. 607-613
Citations number
23
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
CANADIAN JOURNAL OF CARDIOLOGY
ISSN journal
0828282X → ACNP
Volume
16
Issue
5
Year of publication
2000
Pages
607 - 613
Database
ISI
SICI code
0828-282X(200005)16:5<607:PPIECH>2.0.ZU;2-S
Abstract
BACKGROUND: In the normal heart, pericardial pressure is greater than previ ously believed. OBJECTIVES: To explore the contribution of pericardial constraint to the el evated left ventricular (LV) end-diastolic pressure in chronic heart failur e (CHF). ANIMALS AND METHODS: Pericardial pressure was measured directly in 11 dogs with CHF. Seven dogs were instrumented with LV and right ventricular microm anometers and epicardial pacing leads, and paced at 240 to 260 beats/min fo r four to seven weeks. After the development of CHF, a left thoracotomy was performed and a flat pericardial balloon was positioned over the LV free w all through a slit in the pericardium. RESULTS: LV end-diastolic pressure was 31+/-9 mmHg, and pericardial pressur e only 7+/-2 mmHg. Nitroglycerin in six dogs decreased LV end-diastolic pre ssure from 33+/-8 to 28+/-7 and peri cardial pressure from 7+/-2 to 6+/-3 m mHg (both P<0.05). Calculated transmural LV end-diastolic pressure also dec reased (26+/-8 to 22+/-7 mmHg, P<0.05). Volume loading in five dogs increas ed LV end-diastolic pressure from 29+/-8 to 42+/-10 mmHg (P<0.05), pericard ial pressure from 6+3 to 12+/-6 mmHg (not significant) and transmural LV en d-diastolic pressure from 23+/-7 to 30+/-7 mmHg (not significant). When the pericardium was opened in three dogs, the LV end-diastolic pressure decrea sed by 5 mmHg. Four previously uninstrumented dogs were studied to exclude the effects of epicardial scarring; LV end-diastolic pressure was 42+/-6 mm Hg and pericardial pressure was 10+/-6 mmHg. CONCLUSION: Pericardial constraint, a prerequisite for pericardially mediat ed ventricular interaction, was not present to the same extent in this mode l of CHF as in acute models, probably reflecting the importance of pericard ial remodelling.