Transverse tubule remodelling in the atrophied left ventricle in right‑sided heart failure

2021 ◽  
Author(s):  
Kevin Howe ◽  
Jacqueline M. Ross ◽  
Denis S. Loiselle ◽  
June-Chiew Han ◽  
David J. Crossman
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Ex Vivo ◽  
Disease Process ◽  
Force Production ◽  
Right Heart Failure ◽  
Left Ventricular ◽  
Significant Loss ◽  
Papillary Muscles ◽  
The Right

Right-sided heart failure is a common consequence of pulmonary arterial hypertension. Overloading the right ventricle results in hypertrophy, which progresses to failure characterised by impaired Ca2+ dynamics and force production that is linked with transverse(t)-tubule remodelling. This also unloads the left ventricle, which consequently atrophies. Experimental left‑ventricular unloading can result in t-tubule remodelling, but it is currently unclear if this occurs in right-sided heart failure. In this work, we studied the monocrotaline (MCT)-induced right heart failure in the rat, using confocal microscopy to investigate cellular remodelling of t-tubules, junctophilin-2 (JPH2), and ryanodine receptor-2 (RyR2). We examined remodelling across tissue anatomical regions of both ventricles: trabeculae, papillary muscles, and free walls. Our analyses demonstrated in MCT hearts significant loss of t-tubule periodicity, disruption of the normal sarcomere striated pattern with JPH2 labelling, and also a disorganised striated pattern of RyR2 - a feature not previously reported in heart failure. Remodelling of JPH2 and RyR2 in the MCT heart was more pronounced in papillary muscles and trabeculae - particularly in the left ventricle, indicating that these anatomical structures, used as ex vivo isolated muscle preparations, are more sensitive to the disease process.

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.

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.

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.

scholarly journals Epigenetics, inflammation and metabolism in right heart failure associated with pulmonary hypertension

2017 ◽  
Vol 7 (3) ◽  
pp. 572-587 ◽  
Author(s):  
Nolwenn Samson ◽  
Roxane Paulin
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Pressure Overload ◽  
Right Heart Failure ◽  
Left Ventricular ◽  
Ventricular Failure ◽  
Pulmonary Arterial ◽  
Ventricle Hypertrophy ◽  
The Right

Right ventricular failure (RVF) is the most important prognostic factor for both morbidity and mortality in pulmonary arterial hypertension (PAH), but also occurs in numerous other common diseases and conditions, including left ventricle dysfunction. RVF remains understudied compared with left ventricular failure (LVF). However, right and left ventricles have many differences at the morphological level or the embryologic origin, and respond differently to pressure overload. Therefore, knowledge from the left ventricle cannot be extrapolated to the right ventricle. Few studies have focused on the right ventricle and have permitted to increase our knowledge on the right ventricular-specific mechanisms driving decompensation. Here we review basic principles such as mechanisms accounting for right ventricle hypertrophy, dysfunction, and transition toward failure, with a focus on epigenetics, inflammatory, and metabolic processes.

Right Heart Function during Left Ventricular Assistance in an Open-Chest Porcine Model of Acute Right Heart Failure

1994 ◽  
Vol 17 (4) ◽  
pp. 224-229 ◽  
Author(s):  
Y. Abe ◽  
K. Kotoh ◽  
P.H. Deleuze ◽  
M. Miyama ◽  
G.J. Cooper ◽  
...  
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Right Heart Failure ◽  
Left Ventricular ◽  
Volume Loading ◽  
Right Heart ◽  
Open Chest ◽  
The Right ◽  
Ventricular Assistance ◽  
Left Ventricular Assistance

Changes in the right ventricular function measured with a thermodilution ejection fraction catheter have been recorded in open-chest normal pigs and pigs with acute right heart failure (RVF) undergoing left ventricular assistance with a pneumatic-sactype device (LVAD). To produce acute right heart failure, 5 pigs underwent ligation of the right ventricular free wall coronary arteries. Compared with normal pigs, cardiac output in ligated pigs fell by 21% (7.5 ± 0.5 vs 9.5 ± 1.2 L/min; p < 0.05) and the right ventricular end diastolic pressure rose (11.4 ± 2.6 vs 5.7 ± 3.6 vs mmHg: p <0.05). With the left ventricular assist device connected, the right atrial pressure was increased to 3, 5, 7, 10 and 12 mmHg by volume loading while maintaining the haematocrit at 35 ± 6%. The right ventricular stroke work index (RVSWI) increased with volume loading in normal pigs. In RVF pigs, RVSWI increased significantly with the LVAD (59.2 ± 5.8 vs 23.5 ± 7.8 mmHg ml/min/kg, p<0.01), approaching that of normal pigs (62.3 ± 4.8 mmHg ml/min/kg). Similar changes were observed in the cardiac output and right ventricular stroke volume. These results show that, in this model of open-chest, mild, acute right heart failure, left ventricular assistance allows right ventricular function to return to normal, despite volume overloading, by decreasing right ventricular after load and increasing right ventricular compliance

P5370Pulmonary pressure overload stimulates cardiac stem or progenitor cell-derived cardiac regeneration in the right ventricular area

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Kanda ◽  
T Nagai ◽  
N Kondou ◽  
K Tateno ◽  
M Hirose ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Progenitor Cell ◽  
Pressure Overload ◽  
Right Heart Failure ◽  
Left Ventricular ◽  
Free Wall ◽  
Right Heart ◽  
The Right

Abstract Introduction and purpose The number of patients with right heart failure due to pulmonary hypertension has been increasing. Although several drugs have reportedly improved pulmonary hypertension, no treatments have been established for decompensated right heart failure. The heart has an innate ability to regenerate, and cardiac stem or progenitor cells (e.g., side population [SP] cells) have been reported to contribute to the regeneration process. However, their contribution to right ventricular pressure overload has not been clarified. Here, this regeneration process was evaluated using a genetic fate-mapping model. Methods and results We used Cre-LacZ mice, in which more than 99.9% of the cardiomyocytes in the left ventricular field were positive for 5-bromo-4-chloro-3-indolyl-β-D-galactoside (X-gal) staining immediately after tamoxifen injection. Then, we performed either a pulmonary binding (PAB) or sham operation on the main pulmonary tract. In the PAB-treated mice, the right ventricular cavity was significantly enlarged (right-to-left ventricular [RV/LV] ratio, 0.24±0.04 in the sham group and 0.68±0.04 in the PAB group). Increased peak flow velocity in the PAB group (1021±80 vs 1351±62 mm/sec) was confirmed by echocardiography. One month after the PAB, the PAB-treated mice had more X-gal-negative (newly generated) cells than the sham mice (94.8±34.2 cells/mm2 vs 23.1±10.5 cells/mm2; p<0.01). The regeneration was biased in the RV free wall (RV free wall, 225.5±198.7 cells/mm2; septal area, 88.9±56.5/mm2; LV lateral area, 46.8±22.0/mm2; p<0.05). To examine the direct effects of PAB on the cardiac progenitor cells, bromodeoxyuridine was administered to the mice daily until 1 week after the PAB operation. Then, the hearts were isolated and SP cells were harvested. The SP cell population increased from 0.65±0.23% in the sham mice to 1.87% ± 1.18% in the PAB-treated mice. Immunostaining analysis revealed a significant increase in the number of BrdU-positive SP cells, from 11.6±2.0% to 44.0±18%, therefore showing SP cell proliferation. Conclusions Pulmonary pressure overload stimulated cardiac stem or progenitor cell-derived regeneration with a RV bias, and SP cell proliferation may partially contribute to this process. Acknowledgement/Funding JSPS KAKENHI Grant Number JP 17K17636, GSK Japan Research Grant 2016

Alterations in ventricular excitability in conscious dogs during development of chronic heart failure

1986 ◽  
Vol 250 (6) ◽  
pp. H1022-H1029 ◽  
Author(s):  
C. W. White ◽  
M. J. Mirro ◽  
D. D. Lund ◽  
D. J. Skorton ◽  
N. G. Pandian ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Time Course ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Maximum Increase ◽  
Electrophysiological Properties ◽  
Cycle Lengths ◽  
The Right

Arrhythmias in patients with heart failure may result from altered electrophysiological properties of the myocardium. To examine changes in ventricular excitability during cardiac failure and to relate these changes to ventricular structural and neurochemical abnormalities, right ventricular failure was produced in dogs by pulmonary artery banding and by creating tricuspid regurgitation. Right and left ventricular excitability thresholds were tested biweekly in heart failure (HF) and sham-operated conscious dogs by means of strength-duration curves (1-40 ms) at basic cycle lengths (BCL) of 300-500 ms until time of death (21-188 days). Marked increases in the excitability threshold of the right ventricle occurred in HF (mean maximum % increase, 205 +/- 42 at BCL 500 ms). Smaller, though significant increases in the left ventricular excitability threshold in HF were also seen (mean maximum % increase 103 +/- 36 at BCL 500 ms). Increases in the excitability threshold of the left as well as the right ventricles occurred, even though ventricular dilation (2-D Echo) was confined to the right ventricle. The time course of changes in the excitability threshold was variable (maximum occurrence at 21 +/- 3 days right ventricle, 23 +/- 11 days left ventricle). Tyrosine hydroxylase activity and norepinephrine content of the right ventricle were markedly depleted at death, when the excitability threshold was high. Similar though nonsignificant trends in reductions of these sympathetic neurochemicals were seen in the left ventricle. Levels of choline acetyltransferase and QNB binding in both ventricles were unaffected.

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.

scholarly journals Surgical Repair of a Giant Aorto–Left Ventricular Fistula

2019 ◽  
Vol 46 (2) ◽  
pp. 133-135
Author(s):  
Charles Mve Mvondo ◽  
Marta Pugliese ◽  
Ellen M. Dailor
Keyword(s):  
Heart Failure ◽  
Surgical Treatment ◽  
Left Ventricle ◽  
Symptom Severity ◽  
Aortic Wall ◽  
Surgical Repair ◽  
Interventricular Septum ◽  
Left Ventricular ◽  
Unusual Condition ◽  
The Right

Aortoventricular fistula, a rare congenital or acquired defect of the aortic wall, is characterized by an abnormal connection between the aorta and one of the ventricles. Symptom severity correlates with the diameter of the fistula and with the acute or chronic timing of presentation. The diagnosis is usually made by using echocardiography, and surgical treatment is necessary to avoid progression to heart failure. We describe the case of a 27-year-old woman who underwent successful surgical repair of an aortoventricular fistula that originated from the right coronary sinus and extended into the left ventricle through the interventricular septum. In addition to the patient's case, we briefly discuss this unusual condition

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