scholarly journals Allometry of left ventricular myocardial innervation

2013 ◽  
Vol 224 (4) ◽  
pp. 518-526 ◽  
Author(s):  
Julia Schipke ◽  
Terry M. Mayhew ◽  
Christian Mühlfeld
Keyword(s):  
Left Ventricular ◽  
Myocardial Innervation

scholarly journals Effect of stellate ganglia stimulation on global and regional left ventricular function as assessed by speckle tracking echocardiography

2013 ◽  
Vol 304 (6) ◽  
pp. H840-H847 ◽  
Author(s):  
Wei Zhou ◽  
Kentaro Yamakawa ◽  
Peyman Benharash ◽  
Olujimi Ajijola ◽  
Daniel Ennis ◽  
...  
Keyword(s):  
Circumferential Strain ◽  
Stellate Ganglion ◽  
Systolic Pressure ◽  
Pressure Change ◽  
Left Ventricular ◽  
Regional Left Ventricular Function ◽  
Myocardial Innervation ◽  
Chronotropic Response ◽  
Stellate Ganglia ◽  
Regional Strain

Left ventricular (LV) twist mechanics and regional strain during cardiac sympathetic efferent activation are poorly understood. The purpose of this study was to compare the effects of left stellate ganglia (LSG) and right stellate ganglia (RSG) stimulation on cardiac twist/untiwst mechanics and regional strain. In nine pigs, echocardiographic imaging and LV pressure-volume measurements were performed before and during unilateral and bilateral stellate ganglion stimulation. LSG and RSG stimulation significantly augmented LV end-systolic pressure by 24% and 22% ( P < 0.01), maximal rate of LV pressure change by 167% and 165% ( P < 0.01), and time constant of LV relaxation by 20% and 12% ( P < 0.01), respectively. RSG stimulation resulted in a greater chronotropic response than LSG stimulation (RSG: 68% vs. LSG: 12%, P < 0.01). Both LSG and RSG stimulation significantly increased global epicardial and endocardial LV rotation and diastolic untwisting rate and reduced the time to peak rotation ( P < 0.05). However, LSG stimulation predominantly increased radial and circumferential strain in the LV inferoseptal, inferior, posterior, and lateral regions, whereas RSG stimulation primarily increased radial and circumferential strain in the anteroseptal, anterior, and lateral LV regions. Stimulation of both stellate ganglia led to a uniform increase in all LV segments. Our data suggest that LSG and RSG stimulation lead to a global increase in LV twist, driven by distinct regional strain heterogeneity that may result from myocardial innervation from the LSG and RSG. These findings provide a better understanding of the global and regional functional consequences of regional myocardial innervation from the LSG and RSG.

Allometry of left ventricular myocardial innervation

2013 ◽  
Vol 177 (1) ◽  
pp. 57-58
Author(s):  
J. Schipke ◽  
C. Mühlfeld
Keyword(s):  
Left Ventricular ◽  
Myocardial Innervation

Relationships between left ventricular sympathetic innervation and diastolic dysfunction: the role of myocardial innervation/perfusion mismatch

2016 ◽  
Vol 25 (4) ◽  
pp. 1101-1109 ◽  
Author(s):  
Alessia Gimelli ◽  
Riccardo Liga ◽  
Francesco Avogliero ◽  
Michele Coceani ◽  
Paolo Marzullo
Keyword(s):  
Diastolic Dysfunction ◽  
Sympathetic Innervation ◽  
Left Ventricular ◽  
Myocardial Innervation

Mitochondria in Cardiomyopathy: Alterations in Size, Number and Internal Structures

1968 ◽  
Vol 26 ◽  
pp. 126-127
Author(s):  
George Hug ◽  
William K. Schubert
Keyword(s):  
Heart Failure ◽  
Biochemical Analysis ◽  
Left Ventricular ◽  
Size Number ◽  
Internal Structures ◽  
Left Ventricular Outflow ◽  
Chest X Ray ◽  
Myocardial Fibers ◽  
Muscle Biopsies ◽  
Needle Liver Biopsy

A white boy six months of age was hospitalized with respiratory distress and congestive heart failure. Control of the heart failure was achieved but marked cardiomegaly, moderate hepatomegaly, and minimal muscular weakness persisted.At birth a chest x-ray had been taken because of rapid breathing and jaundice and showed the heart to be of normal size. Clinical studies included: EKG which showed biventricular hypertrophy, needle liver biopsy which showed toxic hepatitis, and cardiac catheterization which showed no obstruction to left ventricular outflow. Liver and muscle biopsies revealed no biochemical or histological evidence of type II glycogexiosis (Pompe's disease). At thoracotomy, 14 milligrams of left ventricular muscle were removed. Total phosphorylase activity in the biopsy specimen was normal by biochemical analysis as was the degree of phosphorylase activation. By light microscopy, vacuoles and fine granules were seen in practically all myocardial fibers. The fibers were not hypertrophic. The endocardium was not thickened excluding endocardial fibroelastosis. Based on these findings, the diagnosis of idiopathic non-obstructive cardiomyopathy was made.

Intracellular EDEMA does not adversely affect the ability to cryopreserve intact hearts

1993 ◽  
Vol 51 ◽  
pp. 278-279
Author(s):  
CL Hastings ◽  
RD Carlton ◽  
FG Lightfoot ◽  
AF Tryka
Keyword(s):  
Cell Injury ◽  
Median Sternotomy ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Hypoxic Cell ◽  
Free Wall ◽  
Sprague Dawley ◽  
Left Ventricular Free Wall ◽  
Sprague Dawley Rats

The earliest ultrastructural manifestation of hypoxic cell injury is the presence of intracellular edema. Does this intracellular edema affect the ability to cryopreserve intact myocardium? To answer this guestion, a model for anoxia induced intracellular edema (IE) was designed based on clinical intraoperative myocardial preservation protocol. The aortas of 250 gm male Sprague-Dawley rats were cannulated and a retrograde flush of Plegisol at 8°C was infused over 90 sec. The hearts were excised and placed in a 28°C bath of Lactated Ringers for 1 h. The left ventricular free wall was then sliced and the myocardium was slam frozen. Control rats (C) were anesthetized, the hearts approached by median sternotomy, and the left ventricular free wall frozen in situ immediately after slicing. The slam frozen samples were obtained utilizing the DDK PS1000, which was precooled to -185°C in liguid nitrogen. The tissue was in contact with the metal mirror for a dwell time of 20 sec, and stored in liguid nitrogen until freeze dry processing (Lightfoot, 1990).

Ultrastructural observations of the aorta of calves implanted with a mechanical left ventricular assist device

1990 ◽  
Vol 48 (3) ◽  
pp. 834-835
Author(s):  
J P Cassella ◽  
V Salih ◽  
T R Graham
Keyword(s):  
Left Ventricular Assist Device ◽  
Ventricular Assist Device ◽  
Left Ventricular ◽  
Aortic Tissue ◽  
Assist Device ◽  
Ventricular Assist ◽  
Transmission Electron ◽  
Left Ventricular Assist ◽  
Preliminary Study

Left ventricular assist systems are being developed for eventual long term or permanent implantation as an alternative to heart transplantation in patients unsuitable for or denied the transplant option. Evaluation of the effects of these devices upon normal physiology is required. A preliminary study was conducted to evaluate the morphology of aortic tissue from calves implanted with a pneumatic Left Ventricular Assist device-LVAD. Two 3 month old heifer calves (calf 1 and calf 2) were electively explanted after 128 days and 47 days respectively. Descending thoracic aortic tissue from both animals was removed immediately post mortem and placed into karnovsky’s fixative. The tissue was subsequently processed for transmission electron microscopy (TEM). Some aortic tissue was fixed in neutral buffered formalin and processed for routine light microscopy.

Left Ventricular Hypertrophy

2014 ◽  
Vol 19 (2) ◽  
pp. 11-15
Author(s):  
Steven L. Demeter
Keyword(s):  
Risk Factors ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular Mass Index ◽  
Medical Science ◽  
Careful Analysis ◽  
Left Ventricular ◽  
Hypertensive Disease ◽  
Accurate Analysis ◽  
Clear Explanation

Abstract The fourth, fifth, and sixth editions of the AMA Guides to the Evaluation of Permanent Impairment (AMA Guides) use left ventricular hypertrophy (LVH) as a variable to determine impairment caused by hypertensive disease. The issue of LVH, as assessed echocardiographically, is a prime example of medical science being at odds with legal jurisprudence. Some legislatures have allowed any cause of LVH in a hypertensive individual to be an allowed manifestation of hypertensive changes. This situation has arisen because a physician can never say that no component of LVH was not caused by the hypertension, even in an individual with a cardiomyopathy or valvular disorder. This article recommends that evaluators consider three points: if the cause of the LVH is hypertension, is the examinee at maximum medical improvement; is the LVH caused by hypertension or another factor; and, if apportionment is allowed, then a careful analysis of the risk factors for other disorders associated with LVH is necessary. The left ventricular mass index should be present in the echocardiogram report and can guide the interpretation of the alleged LVH; if not present, it should be requested because it facilitates a more accurate analysis. Further, if the cause of the LVH is more likely independent of the hypertension, then careful reasoning and an explanation should be included in the impairment report. If hypertension is only a partial cause, a reasoned analysis and clear explanation of the apportionment are required.

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