93 A hemodynamic challenge in assessment of echocardiographic mitral regurgitation severity

Abstract Mitral regurgitation severity is, in accordance to current recommendations, typically evaluated by echocardiography. Several hemodynamic factors may influence this evaluation, especially systemic arterial blood pressure at the time of echocardiographic evaluation. A 71-year-old woman was admitted in our Cardiology ward with acute decompensated heart failure. She had been previously admitted about 3 months earlier by acute decompensated heart failure, and at that time, admission transthoracic echocardiography (TTE) demonstrated mitral regurgitation, which was evaluated as severe. Systolic systemic arterial blood pressure at the time of that TTE was registered as 135mmHg. For further evaluation of mitral regurgitation mechanism, the patient underwent transoesophageal echocardiography (TEE), and in that exam mitral regurgitation was assessed as only moderate. For that exam, patient was sedated with 5mg of intravenous Midazolam, a drug with known secondary hypotensive effect. Although systemic arterial blood pressure was not described in the TEE report, retrospective analysis of nursery blood pressure records showed that patient was hypotensive during exam with systolic arterial blood pressure of 80-90mmHg. Patients was discharged, and in actual admission, concern was raised that mitral regurgitation could have been underestimated in previous TEE due to reduced afterload caused by the hypotensive effect of sedation. It was then decided to repeat TEE, and, in order to counterpose the hypotensive effect of Midazolam, TEE was performed under intravenous continuous infusion of Phenylephrine, a selective α-1 receptor antagonist with a significant vasopressor effect and minimal effect on cardiac contractility. Systolic systemic arterial blood pressure during this exam was recorded as 135-140mmHg. In this exam mitral regurgitation was confirmed as severe and patient was patient was oriented for mitral valve surgery. DIscussion This case illustrates the importance of assessment of hemodynamic status of the patient during echocardiographic evaluation of mitral regurgitation severity, and presents a pharmacological strategy to compensate hypotensive effects of sedative agents used during TEE.

Download Full-text

Hypotensive, cardiodepressant, and vasorelaxant activities of black currant (Ribes nigrum ‘Ben Sarek’) juice

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2015-0584 ◽

2016 ◽

Vol 94 (10) ◽

pp. 1102-1105 ◽

Cited By ~ 1

Author(s):

Suzana Branković ◽

Bojana Miladinović ◽

Mirjana Radenković ◽

Marija Gočmanac Ignjatović ◽

Milica Kostić ◽

...

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Arterial Blood Pressure ◽

Hypotensive Effect ◽

Rat Aorta ◽

Ribes Nigrum ◽

Black Currant ◽

Arterial Blood ◽

Dose Dependent Decrease ◽

Dose Dependent

The aim of this study was to evaluate the effects of black currant (Ribes nigrum L. ‘Ben Sarek’) juice on the blood pressure and frequency of cardiac contractions, as well as vasomotor responses of rat aortic rings. Arterial blood pressure was measured directly from the carotid artery in the anaesthetized rabbits. The aortic rings were pre-contracted with KCl (80 mmol·L−1), after which black currant juice was added. An intravenous injection of black currant juice (0.33–166.5 mg·kg−1) induced a significant and dose-dependent decrease of rabbit arterial blood pressure and heart rate. The black currant juice decreased arterial blood pressure of rabbit by 22.33% ± 3.76% (p < 0.05) and heart rate by 17.18% ± 2.93% (p < 0.05). Cumulative addition of the black currant juice (0.01–3 mg·mL−1) inhibited concentration-dependent KCl induced contractions of the isolated rat aorta. The black currant juice, at the concentration of 3 mg·mL−1, caused a maximum relaxation of 21.75% ± 3.15% (p < 0.05). These results demonstrate that black currant juice can induce hypotension. The hypotensive effect of the black currant may occur as the consequence of its inhibitory activity on the rate of heart contraction and vasorelaxant effects.

Download Full-text

Chronic regulation of arterial blood pressure by ANP: role of endogenous vasoactive endothelial factors

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1998.275.5.h1826 ◽

1998 ◽

Vol 275 (5) ◽

pp. H1826-H1833 ◽

Cited By ~ 6

Author(s):

L. G. Melo ◽

A. T. Veress ◽

U. Ackermann ◽

H. Sonnenberg

Keyword(s):

Blood Pressure ◽

Enzyme Activity ◽

Arterial Blood Pressure ◽

Natriuretic Peptide ◽

Peripheral Resistance ◽

Cardiovascular Effects ◽

Hypotensive Effect ◽

Synthetic Activity ◽

Arterial Blood

Atrial natriuretic peptide (ANP) exerts a chronic hypotensive effect due to a decrease in total peripheral resistance (TPR). This study examines if chronic ANP-dependent vasodilation is attributable to differences in the cardiovascular regulatory activity of vascular endothelium (VE), based on evidence that ANP affects synthesis/release and target cardiovascular effects of endothelin-1 (ET-1), C-type natriuretic peptide (CNP), and nitric oxide (NO). To determine if the synthetic activity of resistance vasculature VE is chronically altered by plasma ANP activity, we measured ET-1, CNP, and endothelial constitutive NO synthase (ecNOS) concentration and total NOS enzyme activity in homogenates of kidney, heart, lung, hindquarter skeletal muscle, and brain from hypotensive transgenic mice with elevated plasma ANP, hypertensive knockout mice (−/−) characterized by the absence of ANP, and the corresponding normotensive wild-type (NT, +/+) mice. Tissue distribution and abundance patterns of ET-1, CNP, ecNOS, and NOS enzyme activity were comparable between the different genotypes and did not differ significantly between mutant and control mice. Antagonism of ETA/B receptors in −/− and +/+ mice in vivo with SB-209670 reduced arterial blood pressure (ABP) significantly and comparably in both genotypes (−27 ± 4 and −25 ± 2% change for −/− and +/+ mice, respectively) independent of any significant changes in heart rate (HR) (−6 ± 8 and −4 ± 4% change for −/− and +/+ mice, respectively). Immunoneutralization of CNP-specific guanylate cyclase-linked receptors (GC-B) with monoclonal antibodies (3G12) increased ABP slightly, but not significantly, by similar relative amounts in both −/− (10 ± 6% change) and +/+ mice (8 ± 3% change), without changing HR significantly (4 ± 1% change for both +/+ and −/− mice). Inhibition of NOS activity (by N G-nitro-l-arginine methyl ester) significantly increased ABP, but the changes were comparable between −/− (53 ± 5% change) and +/+ mice (50 ± 6% change) and occurred in the absence of significant changes in HR (−1 ± 5 and 7 ± 5% change for −/− and +/+ mice, respectively). We conclude that the differences in ABP associated with chronic variations in endogenous ANP activity are not due to alterations in synthesis or responsiveness of the cardiovascular system to the effects of ET-1, CNP, or NO.

Download Full-text