Left ventricular dysfunction induced by chronic alcohol ingestion in rats

1991 ◽  
Vol 261 (1) ◽  
pp. H212-H219 ◽  
Author(s):  
J. M. Capasso ◽  
P. Li ◽  
G. Guideri ◽  
P. Anversa
Keyword(s):  
Left Ventricle ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Wall Stress ◽  
Longitudinal Axis ◽  
Left Ventricular ◽  
Experimental Animals ◽  
Chamber Volume ◽  
The Right ◽  
Myocyte Damage

To determine whether moderate ingestion of alcohol for protracted periods of time affects normal cardiac performance and produces myocyte damage, male Fischer 344 rats at 4 mo of age were given 30% ethanol in their drinking water every day for a period of 8 mo. Experimental animals and age-matched controls were examined hemodynamically and morphometrically at 12 mo of age. Body and cardiac growth were depressed in alcoholic animals by 15 and 12%, respectively. Although left ventricular (LV) weight was reduced by 14% in alcoholic rats, no difference in right ventricular (RV) weight was noted, and consequently the ratio of RV weight to body weight increased by 12%. Systemic arterial pressures as well as LV peak systolic pressure decreased in alcoholic rats despite an unchanged heart rate. Myocardial contractility in alcoholic rats was further depressed as revealed by a significant decrease in the peak rate of ventricular pressure decay. Importantly, end-diastolic pressure was elevated 5.2-fold in the left ventricle and 2.9-fold in the right ventricle after 8 mo of ethanol consumption. LV diastolic chamber volume increased through myocardial remodeling as the longitudinal axis and transverse diameters from the base to the apex increased in experimental animals while the thickness of the LV diminished. Structural and hemodynamic alterations resulted in a 571% increase in the volume of diastolic circumferential wall stress on the left ventricle. Damage to the myocardium was increased in alcoholic animals with the volume percent of myocardial lesions increasing 342% in the wall of the left ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventricular systolic interdependence: volume elastance model in isolated canine hearts

1987 ◽  
Vol 253 (6) ◽  
pp. H1381-H1390 ◽  
Author(s):  
W. L. Maughan ◽  
K. Sunagawa ◽  
K. Sagawa
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Cross Talk ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Free Wall ◽  
Right Ventricular Free Wall ◽  
Systolic Volume ◽  
The Right

To analyze the interaction between the right and left ventricle, we developed a model that consists of three functional elastic compartments (left ventricular free wall, septal, and right ventricular free wall compartments). Using 10 isolated blood-perfused canine hearts, we determined the end-systolic volume elastance of each of these three compartments. The functional septum was by far stiffer for either direction [47.2 +/- 7.2 (SE) mmHg/ml when pushed from left ventricle and 44.6 +/- 6.8 when pushed from right ventricle] than ventricular free walls [6.8 +/- 0.9 mmHg/ml for left ventricle and 2.9 +/- 0.2 for right ventricle]. The model prediction that right-to-left ventricular interaction (GRL) would be about twice as large as left-to-right interaction (GLR) was tested by direct measurement of changes in isovolumic peak pressure in one ventricle while the systolic pressure of the contralateral ventricle was varied. GRL thus measured was about twice GLR (0.146 +/- 0.003 vs. 0.08 +/- 0.001). In a separate protocol the end-systolic pressure-volume relationship (ESPVR) of each ventricle was measured while the contralateral ventricle was alternatively empty and while systolic pressure was maintained at a fixed value. The cross-talk gain was derived by dividing the amount of upward shift of the ESPVR by the systolic pressure difference in the other ventricle. Again GRL measured about twice GLR (0.126 +/- 0.002 vs. 0.065 +/- 0.008). There was no statistical difference between the gains determined by each of the three methods (predicted from the compartment elastances, measured directly, or calculated from shifts in the ESPVR). We conclude that systolic cross-talk gain was twice as large from right to left as from left to right and that the three-compartment volume elastance model is a powerful concept in interpreting ventricular cross talk.

Congestive Heart Failure in Copper-Deficient Mice

2003 ◽  
Vol 228 (7) ◽  
pp. 811-817 ◽  
Author(s):  
Laila Elsherif ◽  
Raymond V. Ortines ◽  
Jack T. Saari ◽  
Y. James Kang
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Left Ventricle ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Experimental Models ◽  
Left Ventricular ◽  
Mouse Heart ◽  
Total Period

Copper Deficiency (CuD) leads to hypertrophic cardiomyopathy in various experimental models. The morphological, electrophysiological, and molecular aspects of this hypertrophy have been under investigation for a long time. However the transition from compensated hypertrophy to decompensated heart failure has not been investigated in the study of CuD. We set out to investigate the contractile and hemodynamic parameters of the CuD mouse heart and to determine whether heart failure follows hypertrophy in the CuD heart. Dams of FVB mice were fed CuD or copper-adequate (CuA) diet starting from the third day post delivery and the weanling pups were fed the same diet for a total period of 5 weeks (pre- and postweanling). At week 4, the functional parameters of the heart were analyzed using a surgical technique for catheterizing the left ventricle. A significant decrease in left ventricle systolic pressure was observed with no significant change in heart rate, and more importantly contractility as measured by the maximal rate of left ventricular pressure rise (+dP/dt) and decline (−dP/dt) were significantly depressed in the CuD mice. However, left ventricle end diastolic pressure was elevated, and relaxation was impaired in the CuD animals; the duration of relaxation was prolonged. In addition to significant changes in the basal level of cardiac function, CuD hearts had a blunted response to the stimulation of the β-adrenergic agonist isoproterenol. Furthermore, morphological analysis revealed increased collagen accumulation in the CuD hearts along with lipid deposition. This study shows that CuD leads to systolic and diastolic dysfunction in association with histopathological changes, which are indices commonly used to diagnose congestive heart failure.

scholarly journals Novel Neuromodulation Approach to Improve Left Ventricular Contractility in Heart Failure

2020 ◽  
Vol 13 (11) ◽  
Author(s):  
Vivek Y. Reddy ◽  
Jan Petrů ◽  
Filip Málek ◽  
Lee Stylos ◽  
Steve Goedeke ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Artery ◽  
Diastolic Pressure ◽  
Acute Decompensated Heart Failure ◽  
Systolic Pressure ◽  
Decompensated Heart Failure ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Right Pulmonary Artery ◽  
The Right

Background: Morbidity and mortality outcomes for patients admitted for acute decompensated heart failure are poor and have not significantly changed in decades. Current therapies are focused on symptom relief by addressing signs and symptoms of congestion. The objective of this study was to test a novel neuromodulation therapy of stimulation of epicardial cardiac nerves passing along the posterior surface of the right pulmonary artery. Methods: Fifteen subjects admitted for defibrillator implantation and ejection fraction ≤35% on standard heart failure medications were enrolled. Through femoral arterial access, high fidelity pressure catheters were placed in the left ventricle and aortic root. After electro anatomic rendering of the pulmonary artery and branches, either a circular or basket electrophysiology catheter was placed in the right pulmonary artery to allow electrical intravascular stimulation at 20 Hz, 4 ms pulse width, and ≤20 mA. Changes in maximum positive dP/dt (dP/dt Max ) indicated changes in ventricular contractility. Results: Of 15 enrolled subjects, 5 were not studied due to equipment failure or abnormal pulmonary arterial anatomy. In the remaining subjects, dP/dt Max increased significantly by 22.6%. There was also a significant increase in maximum negative dP/dt (dP/dt Min ), mean arterial pressure, systolic pressure, diastolic pressure, and left ventricular systolic pressure. There was no significant change in heart rate or left ventricular diastolic pressure. Conclusions: In this first-in-human study, we demonstrated that in humans with stable heart failure, left ventricular contractility could be accentuated without an increase in heart rate or left ventricular filling pressures. This benign increase in contractility may benefit patients admitted for acute decompensated heart failure.

Dimensional analysis of the left ventricle: effects of acute aortic regurgitation

1975 ◽  
Vol 228 (2) ◽  
pp. 536-542 ◽  
Author(s):  
SJ Leshin ◽  
LD Horwitz ◽  
JH Mitchell
Keyword(s):  
Left Ventricle ◽  
Aortic Regurgitation ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Systolic Volume ◽  
Severe Aortic Regurgitation ◽  
End Diastolic Volume ◽  
Catheter Technique ◽  
End Systolic Volume

The effects of acute severe aortic regurgitation on the left ventricle were investigated in conscious, chronically instrumented dogs. Left ventricular dimensions and volumes were measured from biplane cineradiographs of beads positioned near the endocardium. Data were collected before and after the production of aortic regurgitation by a catheter technique. The aortic regurgitation resulted in increases in mean aortic pulse pressure from 44 to 73 mmHg (P smaller than 0.001), heart rate from 87 to 122 beats/min (P smaller than 0.02), and left ventricular end-diastolic pressure from 11 to 25 mmHg (P smaller than 0.05). Mean end-diastolic volume rose from 61 to 69 cc (P smaller than 0.001), while end-systolic volume remained unchanged at 37 cc. The end-diastolic dilatation following regurgitation was asymmetrical in that the increase in size was due principally to an increase in the septal-lateral axis. The acute volume load of aortic regurgitation was accomplished by an increase in end-diastolic volume, i.e., the Frank-Starling mechanism. The tachycardia probably reflects augmented cardiac sympathetic activity, but the constant end-systolic volume at a similar mean systolic pressure suggests that the net contractile state was unchanged.

scholarly journals A misinterpretation of the left ventricular non-compactionadult patient with primary pulmonary hypertension

2011 ◽  
Vol 64 (11-12) ◽  
pp. 597-599 ◽  
Author(s):  
Aleksandra Nikolic ◽  
Ljiljana Jovovic ◽  
Velibor Ristic ◽  
Dejan Nikolic ◽  
Lazar Angelkov
Keyword(s):  
Pulmonary Hypertension ◽  
Left Ventricle ◽  
Primary Pulmonary Hypertension ◽  
Systolic Pressure ◽  
Apical Part ◽  
Left Ventricular ◽  
History Of ◽  
Dimensional Echocardiography ◽  
The Right ◽  
Two Dimensional Echocardiography

Non-compaction of the left ventricle is a rare cardiac malformation, defined as a primary cardiomyopathy caused by genetic malformations. Although the pathogenesis of this cardiomyopathy is unknown, there are two possible hypotheses (congenital and acquired) which lead to arrest in intrauterine endomyocardial morphogenesis. We are presenting a case of a 60-year-old woman, with a history of bradyarrhythmia, syncope and cyanosis. Two-dimensional echocardiography showed the thickened myocardium with prominent trabeculations and deep intertrabecular recesses in the two thirds of the apical part of left ventricle walls. The right side cavity was enlarged with hypertrophied wall. Tricuspid regurgitation was moderate. Systolic pressure in the right ventricle was 70mmHg. Catheterization of the right heart showed high pressure in the pulmonary artery. According to publications, this is a very rare case with the presence of possible primary pulmonary hypertension and non-compaction of the left ventricle.

Trabecular cutting: a novel surgical therapy to increase diastolic compliance

2019 ◽  
Vol 127 (2) ◽  
pp. 457-463
Author(s):  
Meagan Oglesby ◽  
Danny Escobedo ◽  
Gladys Patricia Escobar ◽  
Fatemeh Fatemifar ◽  
Edward Y. Sako ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Diastolic Pressure ◽  
Ex Vivo ◽  
Systolic Function ◽  
Wall Stress ◽  
Rabbit Heart ◽  
Left Ventricular ◽  
Before And After ◽  
Diastolic Compliance

Heart failure with preserved ejection fraction (HFpEF) is a common cause of hospital admission in patients over 65 yr old and has high mortality. HFpEF is characterized by left ventricular (LV) hypertrophy that reduces compliance. Current HFpEF therapies control symptoms, but no existing medications or therapies can sustainably increase LV compliance. LV trabeculae develop hypertrophy and fibrosis that contribute to reduced LV compliance. This study expands our previous results in ex vivo human hearts to show that severing LV trabeculae increases diastolic compliance in an ex vivo working rabbit heart model. Trabecular cutting was performed in ex vivo rabbit hearts set up in a working heart perfusion system perfused with oxygenated Krebs-Henseleit buffer. A hook was inserted in the LV to cut trabeculae. End-systolic and end-diastolic pressure-volume relationships during transient preload reduction were recorded using an admittance catheter in the following three groups: control (no cutting; n = 9), mild cutting (15 cuts; n = 5), and aggressive cutting (30 cuts; n = 5). In a second experiment, each heart served as its own control. Hemodynamic data were recorded before and after trabecular cutting ( n = 10) or sham cutting ( n = 5) within the same heart. In the first experiments, trabecular cutting did not affect systolic function ( P > 0.05) but significantly increased overall diastolic compliance ( P = 0.009). Greater compliance was seen as trabecular cutting increased ( P = 0.002, r2 = 0.435). In the second experiment, significant increases in systolic function ( P = 0.048) and diastolic compliance ( P = 0.002) were seen after trabecular cutting compared with baseline. In conclusion, trabecular cutting significantly increases diastolic compliance without reducing systolic function. NEW & NOTEWORTHY We postulate that, in mammalian hearts, free-running trabeculae carneae exist to provide tensile support to the left ventricle and minimize diastolic wall stress. Because of hypertrophy and fibrosis of trabeculae in patients with left ventricular hypertrophy, this supportive role can become pathologic, worsening diastolic compliance. We demonstrate a novel operation involving cutting trabeculae as a method to acutely increase diastolic compliance in patients presenting with heart failure and diastolic dysfunction to improve their left ventricle compliance.

Abstract 30: Incomplete Chest Recoil During Piglet CPR Worsens Hemodynamics

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Mathias Zuercher ◽  
Ronald W Hilwig ◽  
Jon Nysaether ◽  
Vinay M Nadkarni ◽  
Marc D Berg ◽  
...  
Keyword(s):  
Blood Flow ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Right Atrial ◽  
Coronary Perfusion ◽  
Parametric Data ◽  
Wilcoxon Rank Sum Test ◽  
The Right

Background : Incomplete chest recoil during cardiopulmonary resuscitation (CPR) (ie, leaning on the chest during the decompression phase) is purported to decrease venous return, and thereby decrease forward blood flow. Aim To determine the effect of 10% and 20% lean on hemodynamics during piglet CPR. Methods : 10 piglets (10.7±1.2 kg) were anesthetized with isoflurane and instrumented with micromanometer-tipped catheters in the right atrium (RA) and aorta (Ao). After induction of ventricular fibrillation, CPR was provided in three-minute epochs with no lean, 10% lean, or 20% lean while aortic systolic pressure (AoS) was targeted at 80–90 mmHg. Because the mean force to attain 80 –90 mm Hg AoS was 18 kg in preliminary studies, 10% and 20% lean were provided as 1.8 and 3.6 kg weights on the chest, respectively. Left ventricular myocardial blood flow (MBF) and cardiac index (CI) were determined by fluorescent, color-microsphere technique. Statistics: paired t -test and repeated measurement ANOVA for parametric, Wilcoxon Rank Sum Test and Friedman’s ANOVA for non-parametric data. Results : 10% and 20% lean resulted in higher right atrial diastolic pressure (RAD) and lower coronary perfusion pressure (CPP) than no lean. Hemodynamics were not different with 10% lean vs. 20% lean. Mean 10%–20% lean resulted in substantially lower MBF and CI than no lean (Table ). Conclusions : 10–20% leaning during CPR increases RAD, decreases CPP, and substantially decreases MBF and CI. Table

Myocardial perfusion in compensated and failing hypertrophied left ventricle

1985 ◽  
Vol 249 (3) ◽  
pp. H534-H539 ◽  
Author(s):  
D. G. Parrish ◽  
W. S. Ring ◽  
R. J. Bache
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Systolic Pressure ◽  
Weight Ratio ◽  
Wall Stress ◽  
Left Ventricular ◽  
Ventricular Systolic Pressure ◽  
Ventricular Wall Thickness ◽  
Left Ventricular Systolic Pressure ◽  
Increased Blood Flow

This study examined blood flow in the hypertrophied left ventricle with and without failure. Left ventricular hypertrophy was produced in 20 dogs by banding the ascending aorta at 6-7 wk of age; studies were performed after animals reached adulthood. Sixteen dogs had compensated hypertrophy, while four dogs had cardiac failure manifested by left ventricular dilatation and end-diastolic pressures greater than 18 mmHg. The degree of hypertrophy, assessed by left ventricular-to-body weight ratio, was similar in animals with compensated hypertrophy (7.29 +/- 0.26 g/kg) and failure (8.45 +/- 0.15); both were greater than control (4.50 +/- 0.15, P less than 0.01). Left ventricular systolic pressure was similar in compensated hypertrophy (184 +/- 9 mmHg) and failure (226 +/- 29), as compared with control (130 +/- 4; P less than 0.01). Left ventricular blood flow measured with microspheres was 0.89 +/- 0.07 ml X min-1 X g-1 in control animals, was increased to 1.34 +/- 0.05 with compensated hypertrophy (P less than 0.001), and was further increased with failure to 1.86 +/- 0.40 (P less than 0.05). The left ventricular wall thickness-to-cavity diameter ratio was increased to 0.63 +/- 0.04 with compensated hypertrophy but was only 0.40 +/- 0.05 in dogs with failure (P less than 0.01), suggesting that wall stress was greater in hearts with failure. These data suggest that increased blood flow rates in dogs with failure resulted from increased myocardial O2 requirements due to increased systolic wall stress. Need for increased blood flow during resting conditions in dogs with failure would impair the ability for further coronary vasodilation during periods of cardiac stress.

Sympathetic augmentation of cardiac function in developing hypertension in conscious dogs

1988 ◽  
Vol 255 (6) ◽  
pp. H1525-H1534 ◽  
Author(s):  
R. J. Gelpi ◽  
L. Hittinger ◽  
A. M. Fujii ◽  
V. M. Crocker ◽  
I. Mirsky ◽  
...  
Keyword(s):  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Wall Stress ◽  
Left Ventricular ◽  
Rate Of Change ◽  
Conscious Dogs ◽  
Lv Function ◽  
Adrenergic Blockade ◽  
Mean Velocity ◽  
Major Mechanism

To determine the alterations in left ventricular (LV) function and the mechanisms involved that occur during the development of perinephritic hypertension, dogs were instrumented with a miniature LV pressure transducer, aortic and left atrial catheters, and ultrasonic crystals to measure LV diameter in the short and long axes and wall thickness. At 2 wk after initiation of perinephritic hypertension, increases (P less than 0.05) were observed in LV systolic pressure, LV end-diastolic pressure, both short- and long-axis end-diastolic diameters, calculated LV end-diastolic volume, stroke volume, global average LV systolic wall stress, first derivative of LV pressure (LV dP/dt), and ejection fraction, whereas mean velocity of circumferential fiber shortening (Vcf) and rate of change of LV short-axis diameter (LV dD/dt) rose but not significantly. At three levels of matched preload and afterload induced by the administration of graded doses of phenylephrine, Vcf, LV dD/dt, and LV dP/dt increased in hypertension compared with the same levels of preload and afterload before hypertension. When the loading conditions in the normotensive and hypertensive dogs were matched, either after ganglionic blockade or beta-adrenergic blockade, both isovolumic and ejection-phase indexes of LV function remained similar before and after hypertension. Thus we conclude that 1) LV function in intact, conscious dogs with early hypertension is enhanced, and 2) the major mechanism for the increase in LV function involves the sympathetic nervous system.

Pattern of function of left ventricle of mammals

1965 ◽  
Vol 209 (1) ◽  
pp. 22-32 ◽  
Author(s):  
J. P. Holt ◽  
Helga Kines ◽  
E. A. Rhode
Keyword(s):  
Left Ventricle ◽  
Stroke Volume ◽  
Systolic Pressure ◽  
Wall Stress ◽  
Limited Range ◽  
Left Ventricular ◽  
Elasticity Constant ◽  
Systolic Volume ◽  
Total Potential ◽  
Internal Volume

Since, over a limited range, rubber has elastic properties similar to contracted cardiac muscle, a method for determining the elasticity constant of rubber left ventricle models has been developed and used to determine the elasticity constant of the contracted mammalian left ventricle. Serial determinations of left ventricular end-systolic pressure, enddiastolic volume, end-systolic volume, and stroke volume were carried out following increased blood volume and stepwise hemorrhages in rabbits, dogs, swine, horses, and cattle. The end-systolic pressure-volume relationship of the ventricle of these animals was found to be similar to that of rubber ventricle models, hemiprolate spheroids, and thick-walled spheres; evidence is presented that the contracted left ventricle, and rubber models of it, function as an equivalent thick-walled sphere having the same wall mass and internal volume. From the linear relationship between "average" wall stress and "average" circumference, equations are derived relating chamber internal volume and: systolic pressure, total potential energy, and energy dissipated in ejection of the stroke volume.

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