Application of cine nuclear magnetic resonance imaging for sequential evaluation of response to angiotensin-converting enzyme inhibitor therapy in dilated cardiomyopathy

Doherty, Neil E.; Seelos, Klaus; Suzuki, Jun; Caputo, Gary R.; O’Sullivan, Margaret; Sobol, Samuel M.; Cavero, Patricia G.; Chatterjee, Kanu; Parmley, William W.; Higgins, Charles B.

doi:10.1016/0735-1097(92)90337-m

Cited by 87 publications

(21 citation statements)

References 38 publications

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“…Since diastolic filling is less abnormal in female rats to begin with, treatments which have a major influence on LV filling characteristics may not be as effective. In addition, ACE inhibitors are known to decrease LV mass after MI or in other forms of heart failure [45, 46, 47]. Again, since females appear to have less reactive hypertrophy of the noninfarcted myocardium, growth-limiting agents may not be beneficial.…”

Section: Discussionmentioning

confidence: 99%

Gender Differences in Postinfarction Left Ventricular Remodeling

Se²,

Litwin³

et al. 1999

Cardiology

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Objective: Previous studies suggest that gender affects the adaptive responses of the heart to some forms of cardiac overload. It is unknown whether gender influences left ventricular (LV) remodeling after myocardial infarction (MI). Methods: We performed transthoracic echocardiographic-Doppler examinations in age-matched male (n = 17) and female (n = 16) rats before, and 1 and 6 weeks after transmural MI or sham surgery. Results: Following large MI (male = 45 ± 1% LV circumference vs. female = 48 ± 4%, p = NS), both male and female rats developed progressive LV dilatation. Infarctions caused a similar degree of global and regional LV systolic dysfunction in males and females. Male rats had significant increases in the thickness of the noninfarcted posterior wall by 6 weeks after MI. However, posterior wall thickness did not change in the infarcted female rats. Average myocyte diameter in the noninfarcted region of the heart was also greater in male than female MI rats. The combination of increased cavity size with little change in wall thickness resulted in a greater decline in relative wall thickness in the female rats compared to the males. Male rats with MI showed progressively restricted LV diastolic filling as assessed by transmitral Doppler recordings. Female rats had less of an increase in the ratio of early to late transmitral velocities and less of an increase in the E wave deceleration rate after MI. Conclusions: Female rats showed a different pattern of LV remodeling than males with less of an increase in thickness of the noninfarcted portions of the left ventricle than males, but comparable LV cavity enlargement and systolic dysfunction. Despite similar infarct size, females developed less pronounced abnormalities of LV diastolic filling. We hypothesize that the gender-related differences in postinfarction LV remodeling may contribute to the different LV filling patterns, and might ultimately relate to differences in clinical outcome.

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Section: Discussionmentioning

confidence: 99%

Gender Differences in Postinfarction Left Ventricular Remodeling

Se²,

Litwin³

et al. 1999

Cardiology

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“…Assessment of left ventricular volume and ejection fraction can be done by several invasive or non-invasive techniques including contrast angiography [6], radionucide angiography [7], nuclear magnetic resonance imaging [8] and echocardiography [9].…”

Section: Introductionmentioning

confidence: 99%

Reproducibility of left ventricular size, shape and mass with echocardiography, magnetic resonance imaging and radionuclide angiography in patients with anterior wall infarction

et al. 1996

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After myocardial infarction, left ventricular volume and ejection fraction can be assessed by echocardiography, magnetic resonance imaging and radionuclide angiography to guide therapy and determine prognosis. Whether a measured parameter gives the same results irrespective of the method used and the observer who performs the analysis is only partly known. Intra-observer and inter-observer variability were determined for echo and magnetic resonance imaging. Left ventricular ejection fraction measured by these techniques was related to radionuclide angiograms performed in the same period. Intra-observer variability for both echo and MRI was low and in most instances below 5%. Inter-observer variability for the echo and MRI measurements were substantially higher than intra-observer variability. Comparison of the three imaging modalities revealed systematic differences. Therefore, in clinical studies, left ventricular volume and function parameters have to be measured with the same technique and by the same observer in qualified core laboratories.

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“…7 Imaging of the cardiac autonomic nervous system has recently entered large-scale clinical trials and has supported a prognostic value in HF. 111,112 Interventions Targeting the Autonomic Nervous System in HF Pharmacological Blockade of the SNS β-blockers reverse ventricular remodeling 113,114 and reduce mortality in patients with HF. [115][116][117] The use of 1 of the 3 β blockers proven to reduce mortality (eg, bisoprolol, carvedilol, and sustained-release metoprolol succinate) is, therefore, recommended for all patients with current or previous symptoms of HF with reduced EF.…”

Section: Imaging Of Cardiac Sympathetic Nerve Terminalsmentioning

confidence: 99%

The Autonomic Nervous System and Heart Failure

Florea

Cohn

2014

Circulation Research

439

366

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Abstract:The pathophysiology of heart failure (HF) is characterized by hemodynamic abnormalities that result in neurohormonal activation and autonomic imbalance with increase in sympathetic activity and withdrawal of vagal activity. Alterations in receptor activation from this autonomic imbalance may have profound effects on cardiac function and structure. Inhibition of the sympathetic drive to the heart through β-receptor blockade has become a standard component of therapy for HF with a dilated left ventricle because of its effectiveness in inhibiting the ventricular structural remodeling process and in prolonging life. Several devices for selective modulation of sympathetic and vagal activity have recently been developed in an attempt to alter the natural history of HF. The optimal counteraction of the excessive sympathetic activity is still unclear. A profound decrease in adrenergic support with excessive blockade of the sympathetic nervous system may result in adverse outcomes in clinical HF. In this review, we analyze the data supporting a contributory role of the autonomic functional alterations on the course of HF, the techniques used to assess autonomic nervous system activity, the evidence for clinical effectiveness of pharmacological and device interventions, and the potential future role of autonomic nervous system modifiers in the management of this syndrome. (Circ Res. 2014;114:1815-1826.) Key Words: autonomic nervous system ■ heart failure ■ norepinephrine ■ receptors, adrenergicThe Autonomic Nervous System and Heart Failure Viorel G. Florea, Jay N. Cohn This Review is in a thematic series on The Autonomic Nervous System and the Cardiovascular System, which includes the following articles: Role of the Autonomic Nervous System in Modulating Cardiac Arrhythmias [Circ Res. 2014;114:1004-1021 The Autonomic Nervous System and Hypertension [Circ Res. 2014;114:1804-1814 The Autonomic Nervous System and Heart Failure Renal Denervation for the Treatment of Cardiovascular High Risk-Hypertension or Beyond? Original received February 10, 2014; revision received April 29, 2014; accepted April 29, 2014. In March 2014, the average time from submission to first decision for all original research papers submitted to Circulation Research was 12.63 days.From the Minneapolis VA Health Care System, Section of Cardiology (V.G.F.) and Rasmussen Center for Cardiovascular Disease Prevention, Department of Medicine (J.N.C.), University of Minnesota Medical School.Correspondence to Jay N. endocardium. Parasympathetic effects are carried by the right and left vagus nerves, originating in the medulla. The vagus nerve further divides into the superior and inferior cardiac nerves, finally merging with the postganglionic sympathetic neurons to form a plexus of nerves at the base of the heart, known as the cardiac plexus. 1The 2 mediators of the SNS, norepinephrine and epinephrine, derive from 2 major sources in the body: the sympathetic nerve endings, which release norepinephrine directly into the synaptic cleft, and the adren...

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Application of cine nuclear magnetic resonance imaging for sequential evaluation of response to angiotensin-converting enzyme inhibitor therapy in dilated cardiomyopathy

Cited by 87 publications

References 38 publications

Gender Differences in Postinfarction Left Ventricular Remodeling

Gender Differences in Postinfarction Left Ventricular Remodeling

Reproducibility of left ventricular size, shape and mass with echocardiography, magnetic resonance imaging and radionuclide angiography in patients with anterior wall infarction

The Autonomic Nervous System and Heart Failure

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