scholarly journals Age-associated Decline in Phosphorylated Connexin 43 Protein Expression in the Left Ventricular Tissue of Wister Rats

2019 ◽  
pp. 1-8
Author(s):  
Donatus Onukwufor Onwuli ◽  
Sandra A. Jones
Keyword(s):  
Left Ventricle ◽  
Western Blot ◽  
Cardiac Arrhythmia ◽  
Connexin 43 ◽  
The Elderly ◽  
Left Ventricular ◽  
Cardiac Impulse ◽  
Ventricular Tissue ◽  
Connexin Proteins ◽  
The Right

Cardiac arrhythmia affects ~ 6% in those over 65 years of age (old), but with 0.2% occurrence in those of 45 years and below (young). Arrhythmia can result from dysregulation of the cardiac impulse generation and its conduction. Connexin proteins are responsible for cardiac impulse conduction, and phosphorylation of connexin 43 determines its functional ability. In this study, Phosphorylated connexin 43, density and expression were assessed in ventricular tissues from young (6 months old) and old (24 months old) Wister rats, using the techniques of western blot and immunohistochemistry. Results show that phosphorylated Cx43 in the left ventricle of 24 months old rats significantly declined (P=0.04 & 0.01) by method of western blot and immunohistochemistry respectively, but did not differ in the right ventricle. The left ventricle is known to be responsible for cardiac output. This data suggest an age-associated decline in the expression of phosphorylated connexin 43 in the left ventricle, which may play a significant role in the development of cardiac arrhythmia in the elderly.

scholarly journals Hemodynamic Support Using Percutaneous Transfemoral Impella 5.0 and Impella RP for Refractory Cardiogenic Shock

2019 ◽  
Vol 2019 ◽  
pp. 1-6 ◽  
Author(s):  
Pratik K. Dalal ◽  
Amy Mertens ◽  
Dinesh Shah ◽  
Ivan Hanson
Keyword(s):  
Left Ventricle ◽  
Pulmonary Artery ◽  
Cardiogenic Shock ◽  
Ventricular Function ◽  
Standard Of Care ◽  
Left Ventricular ◽  
Biventricular Failure ◽  
Ventricular Support ◽  
The Right ◽  
Flow Pump

Acute myocardial infarction (AMI) resulting in cardiogenic shock continues to be a substantial source of morbidity and mortality despite advances in recognition and treatment. Prior to the advent of percutaneous and more durable left ventricular support devices, prompt revascularization with the addition of vasopressors and inotropes were the standard of care in the management of this critical population. Recent published studies have shown that in addition to prompt revascularization, unloading of the left ventricle with the placement of the Impella percutaneous axillary flow pump can lead to improvement in mortality. Parameters such as the cardiac power output (CPO) and pulmonary artery pulsatility index (PAPi), obtained through pulmonary artery catheterization, can help ascertain the productivity of right and left ventricular function. Utilization of these parameters can provide the information necessary to escalate support to the right ventricle with the insertion of an Impella RP or the left ventricle with the insertion of larger devices, which provide more forward flow. Herein, we present a case of AMI complicated by cardiogenic shock resulting in biventricular failure treated with the percutaneous insertion of an Impella RP and Impella 5.0 utilizing invasive markers of left and right ventricular function to guide the management and escalation of care.

scholarly journals Left ventricular noncompaction—a rare cause of triad: heart failure, ventricular arrhythmias, and systemic embolic events: a case report 

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Despina Toader ◽  
Alina Paraschiv ◽  
Petrișor Tudorașcu ◽  
Diana Tudorașcu ◽  
Constantin Bataiosu ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Magnetic Resonance ◽  
Magnetic Resonance ◽  
Left Ventricle ◽  
Ventricular Arrhythmias ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Left Ventricular Noncompaction ◽  
Ventricular Noncompaction ◽  
The Right

Abstract Background Left ventricular noncompaction is a rare cardiomyopathy characterized by a thin, compacted epicardial layer and a noncompacted endocardial layer, with trabeculations and recesses that communicate with the left ventricular cavity. In the advanced stage of the disease, the classical triad of heart failure, ventricular arrhythmia, and systemic embolization is common. Segments involved are the apex and mid inferior and lateral walls. The right ventricular apex may be affected as well. Case presentation A 29-year-old Caucasian male was hospitalized with dyspnea and fatigue at minimal exertion during the last months before admission. He also described a history of edema of the legs and abdominal pain in the last weeks. Physical examination revealed dyspnea, pulmonary rales, cardiomegaly, hepatomegaly, and splenomegaly. Electrocardiography showed sinus rhythm with nonspecific repolarization changes. Twenty-four-hour Holter monitoring identified ventricular tachycardia episodes with right bundle branch block morphology. Transthoracic echocardiography at admission revealed dilated left ventricle with trabeculations located predominantly at the apex but also in the apical and mid portion of lateral and inferior wall; end-systolic ratio of noncompacted to compacted layers > 2; moderate mitral regurgitation; and reduced left ventricular ejection fraction. Between apical trabeculations, multiple thrombi were found. The right ventricle had normal morphology and function. Speckle-tracking echocardiography also revealed systolic left ventricle dysfunction and solid body rotation. Abdominal echocardiography showed hepatomegaly and splenomegaly. Abdominal computed tomography was suggestive for hepatic and renal infarctions. Laboratory tests revealed high levels of N-terminal pro-brain natriuretic peptide and liver enzymes. Cardiac magnetic resonance evaluation at 1 month after discharge confirmed the diagnosis. The patient received anticoagulants, antiarrhythmics, and heart failure treatment. After 2 months, before device implantation, he presented clinical improvement, and echocardiographic evaluation did not detect thrombi in the left ventricle. Coronary angiography was within normal range. A cardioverter defibrillator was implanted for prevention of sudden cardiac death. Conclusions Left ventricular noncompaction is rare cardiomyopathy, but it should always be considered as a possible diagnosis in a patient hospitalized with heart failure, ventricular arrhythmias, and systemic embolic events. Echocardiography and cardiac magnetic resonance are essential imaging tools for diagnosis and follow-up.

Abstract 408: Thioredoxin-1 Gene Delivery Induces Hemeoxygenase-1 Mediated Myocardial Preservation after Chronic Infarction in Spontaneously Hypertensive Rats

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
SureshVarma Penumathsa ◽  
Srikanth Koneru ◽  
Mahesh Thirunavukkarasu ◽  
Lijun Zhan ◽  
Nilanjana Maulik
Keyword(s):  
Left Ventricle ◽  
Western Blot ◽  
Infarct Size ◽  
Blot Analysis ◽  
Spontaneously Hypertensive Rats ◽  
Left Ventricular ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Thioredoxin 1 ◽  
Lac Z

Hypertension the major risk factor for many cardiovascular diseases is a result of multiple causes along with excessive generation of reactive oxygen species resulting in imbalance of redox status. Thioredoxin-1 (Trx-1) is a redox regulatory multifunctional protein with anti-inflammatory, anti-apoptotic and antioxidant effects. In the present study we investigated the therapeutic potential of Adeno-Trx-1 in spontaneously hypertensive rats (SHR). The rats were assigned to four different groups (n = 24) such as (1) normotensive Wistar Kyoto (WKY) (2) SHR (3) SHR +Adeno-Lac-Z (SHRLac-Z) and (4) SHR +Adeno-Trx-1 (SHRTrx-1). Echo-guided gene delivery to the anterior wall of left ventricle was performed using 1x109 pfu of adenovirus constructed with Trx-1 and Lac-Z. Two days after injection of adeno virus, the hearts were subjected to permanent left anterior descending coronary artery occlusion (MI). Left ventricular functions by Echocardiography were examined after 30 days of MI as the significant changes in left ventricle were observed after 4 weeks of MI. Decreased left ventricular inner diameter (7 vs 9 mm) and increased ejection fraction (52 vs 42 %), fractional shortening (28 vs 22 %) was observed in SHRTrx-1 compared to SHR. Infarct size, cardiomyocyte apoptosis and protein expression profiles (by Confocal and Western blot analysis) were observed at predetermined time points i.e after 24 and 48 hours of MI respectively. Decreased infarct size (52% vs 67%), cardiomyocyte apoptosis by TUNEL assay (161 vs 240) and increased expression of Trx-1 and HO-1 were observed in SHRTrx-1 compared to SHR. Confocal results were also confirmed by Western blot analysis. Results documented increased expression of Trx-1 (1.8 fold) and HO-1 (1.4 fold) in SHRTrx-1 as compared to SHR. In addition, we have also observed increased expression of anti-apoptotic protein Bcl-2 (1.7 fold) in SHRTrx-1 treated group compared SHR. Thus our results demonstrate for the first time that the cardioprotective effect of Adeno-Trx-1 therapy in SHR is Trx-1/HO-1/Bcl-2 mediated and may represent a novel mechanism for therapy against hypertension induced post infarction heart failure.

Regulation of K+ and Ca2+ channels in experimental cardiac failure

1991 ◽  
Vol 261 (6) ◽  
pp. H1979-H1987 ◽  
Author(s):  
M. Gopalakrishnan ◽  
D. J. Triggle ◽  
A. Rutledge ◽  
Y. W. Kwon ◽  
J. A. Bauer ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Cardiac Failure ◽  
Radioligand Binding ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
The Right

To examine the status of ATP-sensitive K+ (K+ATP) channels and 1,4-dihydropyridine-sensitive Ca2+ (Ca2+DHP) channels during experimental cardiac failure, we have measured the radioligand binding properties of [3H]glyburide and [3H]PN 200 110, respectively, in tissue homogenates from the rat cardiac left ventricle, right ventricle, and brain 4 wk after myocardial infarction induced by left coronary artery ligation. The maximal values (Bmax) for [3H]glyburide and [3H]PN 200 110 binding were reduced by 39 and 40%, respectively, in the left ventricle, and these reductions showed a good correlation with the right ventricle-to-body weight ratio in heart-failure rats. The ligand binding affinities were not altered. In the hypertrophied right ventricle, Bmax values for both the ligands were not significantly different when data were normalized to DNA content or right ventricle weights but showed an apparent reduction when normalized to unit protein or tissue weight. Moderate reductions in channel densities were observed also in whole brain homogenates from heart failure rats. Assessment of muscarinic receptors, beta-adrenoceptors and alpha 1-adrenoceptors by [3H]quinuclidinyl benzilate, [3H]dihydroalprenolol, and [3H]prazosin showed reductions in left ventricular muscarinic and beta-adrenoceptor densities but not in alpha 1-adrenoceptor densities, consistent with earlier observations. It is suggested that these changes may in part contribute to the pathology of cardiac failure.

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.

Isolated left ventricular apical hypoplasia in a young child

2021 ◽  
Vol 14 (1) ◽  
pp. e239297
Author(s):  
H Ravi Ramamurthy ◽  
Onkar Auti ◽  
Vimal Raj ◽  
Kiran Viralam
Keyword(s):  
Left Ventricle ◽  
Left Ventricular ◽  
Long Term Outcomes ◽  
Wave Inversion ◽  
St Segment ◽  
Cardiac Apex ◽  
The Right ◽  
First Time ◽  
Left Lead

A 16-month-old, healthy, asymptomatic male child presented with a diagnosis of dilated cardiomyopathy. Cardiovascular examination and chest radiograph were normal. ECG revealed sinus rhythm, and the augmented vector left lead showed raised ST segment, T wave inversion and q waves. Echocardiography showed a globular left ventricle with notched cardiac apex, abnormal echogenicity in the left ventricular apical myocardium, single papillary muscle and normal biventricular function. Cardiac MRI scan revealed a globular left ventricle with fibrofatty changes and retraction of the apex, the papillary muscles closely approximated, and the right ventricle wrapping around the apex of the left ventricle. This is described as isolated left ventricular apical hypoplasia. Diagnosis of this rare entity can be made by MRI, and it has been diagnosed largely in adults. The pathophysiology and long-term outcomes are unknown. We characterise the echocardiography findings of this rare anomaly in a child for the first time in the literature.

scholarly journals Heart anatomy of Giraffa camelopardalis rothschildi: a case report

2008 ◽  
Vol 53 (No. 3) ◽  
pp. 165-168 ◽  
Author(s):  
W. Perez ◽  
M. Lima ◽  
G. Pedrana ◽  
F. Cirillo
Keyword(s):  
Case Report ◽  
Coronary Artery ◽  
Left Ventricle ◽  
Left Coronary Artery ◽  
Left Ventricular ◽  
Left Auricle ◽  
Papillary Muscles ◽  
Atrioventricular Valve ◽  
Heart Anatomy ◽  
The Right

In the present study the most outstanding anatomical findings of the heart of a giraffe are described. Two papillary muscles were found in the right ventricle, namely magnus and subarterial. There were no papillary parvi muscles. The supraventricular crest gave insertion to various tendinous chords. These chords fixed the angular cusp of the right atrioventricular valve. The pectinate muscles were better developed in the left auricle than in the right one. Within the left ventricle two big papillary muscles were found as well as a notorious septomarginal trabecula. The left coronary artery irrigated the majority of the heart’s territory. It gave origin to the interventricular paraconal branch and to the circumflex branch. The latter gave off the branch of the left ventricular border and the interventricular subsinosal branch.

P5272Right versus Left Ventricular Remodelling after Surgical myectomy for HOCM

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Abdelkhalek ◽  
A El Sawy ◽  
R Doss ◽  
A Samaan ◽  
M Donia ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Nyha Class ◽  
Left Ventricular ◽  
P Value ◽  
Peak Strain ◽  
Functional Changes ◽  
Septal Myectomy ◽  
Surgical Myectomy ◽  
The Right

Abstract Background Surgical myectomy for (HOCM) results in complex structural and functional changes. “Remodelling” in different cardiac chambers. To date, changes in the Right versus the left Ventricle have not been studied. Methods Fourty five patients (mean age = 32±16, 68% males) who underwent extended septal myectomy for LVOTO and Fourty “normal” controls (mean age = 32±12 years, 52% males) were studied by cardiac magnetic resonance imaging (CMR). The patients were studied pre-operatively and 6–18 months post-operatively (median = 9 months). The images were analysed by both commercial and in-house software. Results After myectomy. Follow up CMR showed changes in RV mass (21±5 to 23±7) g/m2, volume (60±15 to 66±12) ml/m2 and shape using 3 different methods. RV deformation parameters showed significant changes with circumferential strain (−8±2 to −14±4), filling (38±16 to 62±19) ml/s/m2 and ejection rate (−44±17 to −75±22). Changes in RV were substantially higher than those observed in the LV (Figure. 1, Table. 1). All patients reported significant symptomatic improvement with 31 (78%) patients in NYHA class I and 9 (22%) in class II at follow up. Significant reduction in peak gradient across the LVOT by 75%. Table 1. Summary of reported parameters related to RV Shape for pre and post operation HOCM patients and Normal Healthy Volunteers LV RV Pre Post Normal P-value Pre Post Normal P-value EDV ml/m2 75±18 81±14 73±10 0.005 60±15 66±12 71±12 0.002 ESV ml/m2 20±9 24±8 26±6 0.008 16±7 19±9 26±7 0.02 SV ml/m2 56±13 57±10 51±13 0.38 44±11 48±10 49±14 0.009 EF 74±7 70±7 65±5 0.001 74±8 72±7 64±6 0.228 Mass g/m2 74±33 62±29 27±8 0.0456 21±5 23±7 18±5 0.2100 PFR ml/m2 173±48 141±48 141±40 <0.0001 38±16 62±19 55±24 <0.0001 PER ml/m2 −179±35 −172±42 −144±42 0.29 −44±17 −75±22 −57±22 <0.0001 Peak Strain −20±3 −20±3 −20±3 0.49 −8±2 −14±4 −12±3 <0.0001 Conclusion LV septal myectomy is followed by structural and functional remodelling which is more extensive in the right than the left ventricle. The clinical significance of these findings needs further study.

Immersion before dry simulated dive reduces cardiomyocyte function and increases mortality after decompression

2010 ◽  
Vol 109 (3) ◽  
pp. 752-757 ◽  
Author(s):  
Svein Erik Gaustad ◽  
Alf O. Brubakk ◽  
Morten Høydal ◽  
Daniele Catalucci ◽  
Gianluigi Condorelli ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Survival Time ◽  
Left Ventricular ◽  
Endoplasmic Reticulum Calcium ◽  
Protein Levels ◽  
Left Ventricular Tissue ◽  
Bubble Detection ◽  
Ventricular Tissue ◽  
The Right ◽  
Phospholamban Phosphorylation

Diving and decompression performed under immersed conditions have been shown to reduce cardiac function. The mechanisms for these changes are not known. The effect of immersion before a simulated hyperbaric dive on cardiomyocyte function was studied. Twenty-three rats were assigned to four groups: control, 1 h thermoneutral immersion, dry dive, and 1 h thermoneutral immersion before a dive (preimmersion dive). Rats exposed to a dive were compressed to 700 kPa, maintained for 45 min breathing air, and decompressed linearly to the surface at a rate of 50 kPa/min. Postdive, the animals were anesthetized and the right ventricle insonated for bubble detection using ultrasound. Isolation of cardiomyocytes from the left ventricle was performed and studied using an inverted fluorescence microscope with video-based sarcomere spacing. Compared with a dry dive, preimmersion dive significantly increased bubble production and decreased the survival time (bubble grade 1 vs. 5, and survival time 60 vs. 17 min, respectively). Preimmersion dive lead to 18% decreased cardiomyocyte shortening, 20% slower diastolic relengthening, and 22% higher calcium amplitudes compared with controls. The protein levels of the sarco-endoplasmic reticulum calcium ATPase (SERCA2a), Na+/Ca2+ exchanger (NCX), and phospholamban phosphorylation in the left ventricular tissue were significantly reduced after both dry and preimmersion dive compared with control and immersed animals. The data suggest that immersion before a dive results in impaired cardiomyocyte and Ca2+ handling and may be a cellular explanation to reduced cardiac function observed in humans after a dive.

43Dynamic atrioventricular delay achieves superior electrical synchrony when pacing both ventricles rather than left ventricle alone

EP Europace ◽  
2020 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
B Thibault ◽  
A Chow ◽  
J Mangual ◽  
N Badie ◽  
P Waddingham ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Right Ventricular ◽  
Left Ventricular ◽  
Ventricular Pacing ◽  
Right Ventricular Pacing ◽  
Atrioventricular Delay ◽  
Intrinsic Conduction ◽  
Left Ventricular Pacing ◽  
Additional Reference ◽  
The Right

Abstract Funding Acknowledgements Abbott Introduction Automatic adjustment of atrioventricular delay (AVD) with SyncAV has been shown to improve electrical synchronization when pacing one or two sites in the left ventricle together with the right ventricle. However, it is unknown if the same benefit can be gained by using SyncAV while pacing only the left ventricle without right ventricular pacing. Purpose   Evaluate the acute improvement in electrical synchrony provided by SyncAV with and without MultiPoint Pacing (MPP) during biventricular (BiV) and LV only pacing. Methods   Patients with LBBB and QRS duration (QRSd) ≥ 150 ms scheduled for CRT-P/D device implantation with quadripolar LV lead were enrolled in this prospective study. QRSd was measured post-implant from 12-lead surface electrograms by blinded experts during the following pacing configurations: intrinsic conduction, conventional BiV (BiV = RV + LV1), MPP (MPP = RV + LV1 + LV2), LV-only single-site (LVSS = LV1 only), and LV-only MPP (LVMPP = LV1 + LV2). For each pacing mode, SyncAV was enabled (e.g. BiV + SyncAV) with the patient-tailored SyncAV offset that minimized QRSd. As an additional reference, QRSd during BiV was also measured using the nominal static AVD (paced/sensed AVD = 140/110 ms). BiV and LVSS pacing used the latest activating LV cathode, whereas MPP and LVMPP used the two LV cathodes with the widest possible separation (&gt;30mm). All configurations used the minimum programmable RV-LV and LV1-LV2 delays. Results   Thirty-five patients (78% male, 33% ischemic, 26% ejection fraction, 165 ms intrinsic QRSd) completed device implant and QRSd assessment. Relative to intrinsic conduction, BiV with nominal AVD reduced the QRSd by 17.5% (p &lt; 0.001 vs intrinsic). Enabling SyncAV with a patient-optimized offset significantly improved QRSd reduction. BiV + SyncAV reduced QRSd by 25.2% (p &lt; 0.001 vs. BiV). The greatest QRSd reduction of 28.9% was achieved by MPP + SyncAV (p &lt; 0.01 vs. BiV + SyncAV). Single- and multi-site LV-only pacing reduced QRSd significantly less than corresponding biventricular modes. LVSS + SyncAV reduced QRSd by 22.5% (p &lt; 0.05 vs. BiV + SyncAV), and LVMPP + SyncAV reduced QRSd by 24.3% (p &lt; 0.05 vs. MPP + SyncAV). As a percent of PR interval, optimal SyncAV offsets were similar for BiV + SyncAV (median: 13%, mean: 17%) vs. MPP + SyncAV (median: 13%, mean 16%, p = 0.35 vs. BiV + SyncAV), and similar for LVSS + SyncAV (median: 20%, mean: 28%) and LVMPP + SyncAV (median: 23%, mean: 26%, p = 0.35 vs. LVSS + SyncAV), but were significantly higher for LV-only settings vs. corresponding BiV/MPP settings (p &lt; 0.01 for both pairs). Conclusion: Greater improvement in electrical synchrony using SyncAV was observed when right ventricular pacing was included with left ventricular pacing. Additional benefit was gained by the addition of a second left ventricular pacing site with MPP in combination with SyncAV in both biventricular and LV only pacing modes. Abstract Figure.

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