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

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.

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.

scholarly journals Congestive heart failure in a young cat with excessive moderator bands (false tendons) in the left ventricle

2021 ◽  
Vol 51 (10) ◽  
Author(s):  
Fernanda Genro Cony ◽  
Matheus Viezzer Bianchi ◽  
Fernando Froner Argenta ◽  
Carolina Rodrigues Oliveira ◽  
Carine Stefanello ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Left Ventricle ◽  
Interventricular Septum ◽  
Single Layer ◽  
Left Ventricular ◽  
Pulmonary Atelectasis ◽  
History Of ◽  
Adult Cats ◽  
Well Differentiated

ABSTRACT: Left ventricular false tendons are fibrous or fibromuscular bands that transverse the ventricular cavity and have no attachment to the mitral valve in many species. In cats it is considered a congenital defect that is rarely related to clinical disease and death in adult cats. A 45 days-old mixed breed cat had a history of inappetence since birth. At the physical exam the patient was lethargic and presented restrictive dyspnoea. At necropsy, there were marked ascites, hydrothorax, hepatomegaly with enhanced lobular pattern (nutmeg liver), and the lungs were markedly diminished (compressive pulmonary atelectasis). The heart was enlarged due to marked dilation of the cardiac chambers. Moreover, multiple slightly whitish and irregular cord-like structures were connecting the posterior papillary muscle to the interventricular septum (excessive moderator bands /left ventricular false tendons) at the left ventricle. Microscopically, these structures were characterized by a marked proliferation of fibrous connective tissue intermixed with Purkinje cells and well-differentiated cardiomyocytes lined by a single layer of endocardium. This study described a case of excessive moderator bands (left ventricular false tendons) in a young cat associated with congestive heart failure and death.

Parasympathetic control of the heart. I. An interventriculo-septal ganglion is the major source of the vagal intracardiac innervation of the ventricles

2004 ◽  
Vol 96 (6) ◽  
pp. 2265-2272 ◽  
Author(s):  
Tannis A. Johnson ◽  
Alrich L. Gray ◽  
Jean-Marie Lauenstein ◽  
Stephen S. Newton ◽  
V. John Massari
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Interventricular Septum ◽  
Left Ventricular ◽  
Anterior Surface ◽  
Ventricular Performance ◽  
Neuronal Marker ◽  
Left And Right ◽  
Intracardiac Ganglia ◽  
The Right

The locations, projections, and functions of the intracardiac ganglia are incompletely understood. Immunocytochemical labeling with the general neuronal marker protein gene product 9.5 (PGP 9.5) was used to determine the distribution of intracardiac neurons throughout the cat atria and ventricles. Fluorescence microscopy was used to determine the number of neurons within these ganglia. There are eight regions of the cat heart that contain intracardiac ganglia. The numbers of neurons found within these intracardiac ganglia vary dramatically. The total number of neurons found in the heart (6,274 ± 1,061) is almost evenly divided between the atria and the ventricles. The largest ganglion is found in the interventricular septum (IVS). Retrogradely labeled fluorescent tracer studies indicated that the vagal intracardiac innervation of the anterior surface of the right ventricle originates predominantly in the IVS ganglion. A cranioventricular (CV) ganglion was retrogradely labeled from the anterior surface of the left ventricle but not from the anterior surface of the right ventricle. These new neuroanatomic data support the prior physiological hypothesis that the CV ganglion in the cat exerts a negative inotropic effect on the left ventricle. A total of three separate intracardiac ganglia innervate the left ventricle, i.e., the CV, IVS, and a second left ventricular (LV2) ganglion. However, the IVS ganglion provides the major source of innervation to both the left and right ventricles. This dual innervation pattern may help to coordinate or segregate vagal effects on left and right ventricular performance.

scholarly journals Different reverse remodelling between left ventricle and right ventricle in fulminant heart failure due to giant cell myocarditis: a case report

2021 ◽  
Vol 5 (8) ◽  
Author(s):  
Hiroaki Yokoyama ◽  
Masashi Yamaguchi ◽  
Kazuki Tobita ◽  
Shigeru Saito
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Giant Cell ◽  
Functional Recovery ◽  
Left Ventricular ◽  
Giant Cell Myocarditis ◽  
Reverse Remodelling ◽  
The Right ◽  
Immunosuppression Therapy

Abstract Background Giant cell myocarditis (GCM) is a rare cause of fulminant heart failure (HF). The most common presentation is progressive hemodynamic deterioration, and a few cases present with idiopathic complete atrioventricular block (cAVB). The prognosis of GCM is poor, and GCM patients usually die of HF and ventricular arrhythmia unless cardiac transplantation is performed. Few reports have described the effects of treatments such as immunosuppression and detailed reverse remodelling in GCM patients. Case summary A 69-year-old female presented with cAVB. Transvenous pacemaker was implanted via the left subclavian vein. One and a half months later, she exhibited left ventricular dyssynchrony and lower left ventricular ejection fraction (LVEF), resulting in hospitalization for HF. She received cardiac resynchronization therapy; however, this had no apparently positive effects on her cardiac function. To investigate the cause of the lower LVEF, an endomyocardial biopsy was taken from the right ventricular septum. She was diagnosed with GCM and immediately received immunosuppression therapy with prednisolone and ciclosporin. This resulted in the functional recovery of the right ventricle; on the other hand, the left ventricle had still not recovered based on transthoracic echocardiography. Fortunately, she successfully recovered from severe HF without recurrence. Discussion This is a case of fulminant HF due to GCM which initially presented as cAVB. Moreover, this case demonstrates the quite difference of the functional recovery between the left ventricle and the right ventricle with immunosuppression therapy.

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.

Left Ventricular Myxoma Producing Cardiac Failure

2013 ◽  
Vol 16 (1) ◽  
pp. 57 ◽  
Author(s):  
Erdal Simsek ◽  
Serkan Durdu ◽  
Bledar Hodo ◽  
Levent Yazicioglu ◽  
Adnan Uysalel
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Rare Complication ◽  
Interventricular Septum ◽  
Left Ventricular ◽  
Chronic Obstructive ◽  
Cardiac Tumors ◽  
Obstructive Pulmonary Disease ◽  
Mobile Mass ◽  
Transaortic Approach

<p><b>Introduction:</b> Seventy-five percent of primary cardiac tumors are benign, and most are myxomas. Seventy-five percent of myxomas originate from the left atrium, and 2.5% arise from the left ventricle. Heart failure is a rare complication of myxoma.</p><p><b>Case:</b> A 54-year-old male patient with chronic obstructive pulmonary disease was admitted to the pulmonology department with a diagnosis of pneumonia and congestive heart failure during hospitalization. An echocardiography evaluation revealed a mobile mass (3.3 cm X 1.2 cm) in the left ventricle. The measured ejection fraction was 22%. Transthoracic and transesophageal echocardiography and magnetic resonance imaging examinations confirmed the presence of a myxoma in the left ventricle. The myxoma was a hanging mass with a stalk on the interventricular septum near the anterior mitral valve annulus. We visualized the gelatinous fragile mass on the septum; we then extracted the myxoma via a transaortic approach with the patient on cardiopulmonary bypass. The patient was discharged 10 days after surgery.</p><p><b>Discussion:</b> Myxoma is treated by early surgical resection because of the potential for serious complications. Left ventricular myxomas have been reported to lead to a silent heart failure. This case is important because of its location and the patient's resultant heart failure.</p>

Geometric reconstruction of the left ventricle in lateral wall thrombosis

2020 ◽  
Vol 24 (3) ◽  
pp. 121
Author(s):  
M. D. Alshibaya ◽  
I. V. Slivneva ◽  
M. M. Amirbekov ◽  
Z. M. Cheishvili ◽  
O. S. Lagutina
Keyword(s):  
Surgical Treatment ◽  
Left Ventricle ◽  
Plastic Surgery ◽  
Conflict Of Interest ◽  
Blood Clot ◽  
Interventricular Septum ◽  
Lateral Wall ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Left Ventricular Reconstruction

<p>One variant of postinfarction ischaemic cardiomyopathy is a dyskinetic or akinetic left ventricular aneurysm. Lateral localisation of the postinfarction aneurysms in the interpapillary space is an extremely rare pathology. As a rule, in postinfarction aneurysms of this localization, intracavitary thrombosis develops with large aneurysm sizes or the formation of a false aneurysm. However, thrombus formation in the area of small aneurysms or postinfarction scar of the sidewall, as observed in our case, is extremely rare.<br />This report describes an extremely rare case of the surgical treatment of thrombosis of the posterior-lateral wall of the left ventricle involving the base of the posteromedial papillary muscle.<br />A 59-year-old man was admitted to the hospital with complaints of weakness and shortness of breath under minimal load. He had experienced a heart attack 5 y previously, as per his coronary angiography and had a multi-vessel lesion of the coronary arteries. According to the results of electrocardiography-scarring changes along the posterior wall of the left ventricle, transthoracic echocardiography-dilation of the left heart, a decrease in the ejection fraction of the left ventricle, akinesia of the posterior and posterolateral walls with floating thrombosis of this zone. Surgical intervention was performed under conditions of cardiopulmonary bypass and pharmaco-cryocardioplegia. The heart cavity was opened with left-sided ventriculotomy along the posterior wall, along the interventricular septum. A blood clot was removed with the excision of the lining area along the posterior-lateral wall. Plastic surgery was performed to isolate the scarred myocardium with a Dacron patch; thereafter, reconstruction of the posterior left ventricular wall was performed with a second patch. Plastic surgery of the posterior wall of the left ventricle was performed. The last stage was performed via coronary bypass surgery of the anterior interventricular artery. The duration of stay in the intensive care unit was 20 h, and the duration of hospitalisation was 9 d. He was discharged in the state corresponding to the Class I–II (New York Heart Association Functional Classification, NYHA).<br />Patients with thrombosed left ventricular aneurysms need surgical treatment, irrespective of the localization of the process for de-escalation of the thrombogenic zone and restoration of the ventricle geometry. However, the choice of surgery is clinically challenging and depends on a deep understanding of the anatomical relationships in the left ventricle as well as the prediction of a positive transformation after left ventricular reconstruction. Despite our extensive experience in the treatment of postinfarction aneurysms, this was the first time we treated a patient with an unusual location of a blood clot.</p><p>Received 17 April 2020. Revised 28 May 2020. Accepted 3 June 2020.</p><p><strong>Funding:</strong> The study did not have sponsorship.</p><p><strong>Conflict of interest:</strong> Authors declare no conflict of interest.</p><p><strong>Author contributions</strong><br />Participation in the operation: M.D. Alshibaya, M.M. Amirbekov, Z.M. Cheishvili, O.S. Lagutina, I.V. Slivneva<br />Conception and design: M.D. Alshibaya, I.V. Slivneva<br />Drafting the article: M.D. Alshibaya, I.V. Slivneva, M.M. Amirbekov, Z.M. Cheishvili, O.S. Lagutina<br />Critical revision of the article: M.D. Alshibaya, I.V. Slivneva, M.M. Amirbekov <br />Final approval of the version to be published: M.D. Alshibaya, I.V. Slivneva, M.M. Amirbekov, Z.M. Cheishvili, O.S. Lagutina</p>

scholarly journals D-Shaped Left Ventricle, Anatomic, and Physiologic Implications

2017 ◽  
Vol 2017 ◽  
pp. 1-4 ◽  
Author(s):  
Eder Hans Cativo Calderon ◽  
Tuoyo O. Mene-Afejuku ◽  
Rachna Valvani ◽  
Diana P. Cativo ◽  
Devendra Tripathi ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Interventricular Septum ◽  
Pressure Overload ◽  
Volume Overload ◽  
Left Ventricular ◽  
Transthoracic Echocardiogram ◽  
Elderly Male ◽  
In Series ◽  
The Right

Right ventricular loading/pressure influences left ventricular function because the two ventricles pump in series and because they are anatomically arranged in parallel, sharing the common ventricular septum. Flattening of the interventricular septum detected during echocardiographic examination is called D-shaped left ventricle. We present a case of an elderly male of African descent, who presented with increased shortness of breath. Transthoracic echocardiogram showed flattening and left sided deviation of interventricular septum causing a decreased size in left ventricle, secondary to volume/pressure overload in the right ventricle. While patient received hemodialysis therapy and intravascular volume was removed, patient blood pressure was noted to increase, paradox. Repeated transthoracic echocardiogram demonstrated less left deviation of interventricular septum compared with previous echocardiogram. We consider that it is important for all physicians to be aware of the anatomic and physiologic implication of D-shaped left ventricle and how right ventricle pressure/volume overload affects its function and anatomy.

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