scholarly journals A case of atrial septal defect combined with hypertension and left ventricular hypertrophy. Left ventricular failure induced by balloon occlusion and the effect of nifedipine.

1989 ◽  
Vol 30 (1) ◽  
pp. 103-107 ◽  
Author(s):  
Taku MATSUBARA ◽  
Masaru YAMAZOE ◽  
Takashi KOIKE ◽  
Tohru IZUMI ◽  
Akira SHIBATA
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Atrial Septal Defect ◽  
Ventricular Hypertrophy ◽  
Septal Defect ◽  
Left Ventricular ◽  
Balloon Occlusion ◽  
Left Ventricular Failure ◽  
Ventricular Failure

Restoration of cardiac function and myocardial flow by collateral development in dogs

1981 ◽  
Vol 240 (5) ◽  
pp. H811-H819 ◽  
Author(s):  
M. V. Cohen ◽  
T. Yipintsoi
Keyword(s):  
Left Ventricular ◽  
Balloon Occlusion ◽  
Treadmill Running ◽  
Left Ventricular Failure ◽  
Collateral Flow ◽  
Ventricular Failure ◽  
Hemodynamic Changes ◽  
Group I ◽  
Group Ii ◽  
Myocardial Flow

Hemodynamics of instrumented beagles with 75-85% stenoses of the left circumflex (LCf) coronary artery were evaluated before and during transient LCf balloon occlusion at rest and during treadmill running. Studies were done after surgery and 3 mo later. Myocardial blood flow was measured with radioactive microspheres during the LCf occlusions. Nine dogs (group I) had patent LCf arteries at the second study, and six (group II) had occluded vessels. Transient LCf occlusion during running in group I at weeks 1 and 12 and in group II at week 1 caused significant left ventricular failure, whereas the same protocol in group II dogs at week 12 produced minimal hemodynamic changes. Left ventricular failure precipitated by coronary occlusion during exercise diminished from week 1-12 in those animals with increasing LCf collateral flow, but actually increased in the animals with diminishing collateral flow. In group II dogs after chronic LCf occlusion total flow to LCf myocardium as well as inner-to-outer layer ratios were normal both at rest and during exercise. Thus coronary collaterals do preserve myocardial function, limit adverse hemodynamic responses to myocardial ischemia, and restore postocclusion tissue flows to normal even during the stress of exercise.

Abstract 622: Cd44 Plays an Important Role in Regulating Heart Failure Induced Lung Vascular Remodeling and Who Type-2 Pulmonary Hypertension

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Xinyu Weng ◽  
Wenhui Yue ◽  
Dongzhi Wang ◽  
Huan Wang ◽  
Yawei Xu ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Vascular Remodeling ◽  
Lung Inflammation ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Left Ventricular Failure ◽  
Ventricular Failure

End-stage left ventricular failure or chronic heart failure (CHF) causes severe lung inflammation, vascular remodeling, WHO type-2 pulmonary hypertension, and right ventricular hypertrophy. However, the molecular mechanism of CHF-induced lung inflammation and remodeling is largely unknown. CD44 is a member of the hyaluronate receptor family of cell adhesion molecules, which has been shown to play a selective role in controlling macrophage and lymphocyte migration. Here we demonstrated that end-stage CHF causes a dramatic increase of CD44 expression in heart and lung in human and mice. Histological staining shows that CD44 is predominantly expressed in leukocytes such as macrophages. Flow cytometry analysis further demonstrates that CD44 is predominantly expressed in F4/80 positive macrophages, CD4+, and CD8+ T cells. CD44 expression is dramatically increased in activated T cell subsets. To further determine the physiological role of CD44 in CHF-induced lung remodeling and type-2 pulmonary hypertension, we studied the effect of CD44 blockade on type-2 pulmonary hypertension development in a group of mice with existing moderate left ventricular failure without apparent lung remodeling. Interestingly, we found that blockade CD44 with blocking antibodies (Abs) significantly attenuate the development of lung vascular and interstitial leukocyte infiltration, lung vascular remodeling, fibrosis, and increase of right ventricular hypertrophy. Blockade CD44 signaling also significantly attenuated further decline of left ventricular ejection fraction in mice with existing LV failure. In addition, we demonstrated that induction of T regulatory cells with IL-2 and IL-2 Abs complex significantly attenuated the infiltration of CD44 positive leukocytes in lung tissue, lung vascular remodeling, lung fibrosis, and right ventricular hypertrophy in mice with existing moderate left ventricular failure. Together, these data indicate an important role of CD44 in left ventricular failure-induced lung inflammation, and type-2 pulmonary hypertension, suggesting that inhibition of CD44 may attenuate heart failure progression and type-2 pulmonary hypertension.

Successful Bridge to Heart Transplantation in a Patient with Ebstein's Anomaly

1997 ◽  
Vol 5 (4) ◽  
pp. 239-240
Author(s):  
Mitsuhiro Hachida ◽  
Kazutomo Minami ◽  
Michael Koerner ◽  
Michael Morshuis ◽  
Heinrich Koertke ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Heart Transplantation ◽  
Atrial Septal Defect ◽  
Septal Defect ◽  
Left Ventricular ◽  
Ebstein’S Anomaly ◽  
Mechanical Support ◽  
Tricuspid Valve Replacement ◽  
Ventricular Failure ◽  
Ebstein's Anomaly

A 52-year-old female was diagnosed with Ebstein's anomaly and an associated atrial septal defect. She underwent closure of the atrial septal defect and tricuspid valve replacement. Severe left ventricular failure was found after discontinuation of cardiopulmonary bypass, thus biventricular mechanical support was established. Four days later the patient underwent successful heart transplantation and was discharged without any complications.

Valvar subcoronary aortic stenosis in dogs

1979 ◽  
Vol 236 (5) ◽  
pp. H780-H784
Author(s):  
J. R. Allard ◽  
M. J. O'Neill ◽  
J. I. Hoffman
Keyword(s):  
Survival Rate ◽  
Left Ventricular Hypertrophy ◽  
Aortic Stenosis ◽  
Coronary Arteries ◽  
Heart Block ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Sinus Of Valsalva ◽  
Ventricular Failure ◽  
Valvar Aortic Stenosis

A technique for producing valvar aortic stenosis is described. The noncoronary sinus of Valsalva is plicated externally at a level proximal to the origin of the coronary arteries. The major intraoperative problems are hemorrhage, acute left ventricular failure, and heart block, all of which can be avoided. The survival rate in 26 dogs was 54% and all the survivors remained active. Moderate left ventricular hypertrophy was produced.

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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