Successful Surgical and Anesthetic Management of Vein of Galen Aneurysm in a Neonate in Congestive Heart Failure

Neurosurgery ◽  
1988 ◽  
Vol 22 (5) ◽  
pp. 908-910 ◽  
Author(s):  
Jane Matjasko ◽  
Walker Robinson ◽  
Daniel Eudaily
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Cardiac Failure ◽  
Growth And Development ◽  
Anesthetic Management ◽  
Vascular Supply ◽  
Vein Of Galen ◽  
Vein Of Galen Malformation ◽  
Vein Of Galen Aneurysm

Abstract A 12-day-old infant in intractable cardiac failure due to a vein of Galen malformation was treated successfully with serial ligation of the majority of the vessels feeding the malformation. Despite some residual vascular supply to the malformation, the congestive heart failure has disappeared and growth and development have been normal over a 3-year follow-up period.

scholarly journals Vein of Galen malformation, a rare cause of epilepsy

2016 ◽  
Vol 03 (01) ◽  
pp. 024-025
Author(s):  
Mohammad Sayadnasiri
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Vascular Malformation ◽  
Neonatal Period ◽  
Severe Congestive Heart Failure ◽  
Low Flow ◽  
Vein Of Galen ◽  
Vein Of Galen Malformation ◽  
Venous Structure ◽  
Cerebral Vascular Malformation

AbstractVein of Galen malformation (VOGM) is a rare congenital cerebral vascular malformation characterized by an aneurysmally dilated midline deep venous structure, fed by abnormal arteriovenous communication. Most patients develop severe congestive heart failure at neonatal period that is fatal if left untreated. Rarely, patients with low-flow fistula present with headache, seizure, or focal neurological sign at adulthood. A 28-year-old female with VOGM-related epilepsy was introduced in this brief report.

Vein of Galen malformation presenting as congestive heart failure

2015 ◽  
Vol 08 (04) ◽  
pp. 437-439
Author(s):  
Vinod Maller ◽  
Veena Chowdhury ◽  
Vivek Kottiyath ◽  
Girish Khandelwal ◽  
Rajat Jain ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Vein Of Galen ◽  
Vein Of Galen Malformation

Electrocardiographic changes in patients with cardiac rhabdomyomas associated with tuberous sclerosis

2003 ◽  
Vol 13 (3) ◽  
pp. 258-263 ◽  
Author(s):  
Junko Shiono ◽  
Hitoshi Horigome ◽  
Seiyo Yasui ◽  
Tomoyuki Miyamoto ◽  
Miho Takahashi-Igari ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Left Ventricular Hypertrophy ◽  
Tuberous Sclerosis ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Cardiac Rhabdomyoma ◽  
Ventricular Cavity ◽  
Electrocardiographic Changes

Background:Cardiac rhabdomyomas associated with tuberous sclerosis induce various abnormalities in the electrocardiogram. Electrocardiographic evidence of ventricular hypertrophy may appear if the tumour is electrically active. To our knowledge, electrocardiographic evidence of ventricular hypertrophy has been reported only in association with congestive heart failure. Follow-up studies of changes in electrocardiographic findings are also lacking.Methods:We studied 21 consecutive patients with cardiac rhabdomyoma associated with tuberous sclerosis, 10 males and 11 females, aged from the date of birth to 9 years at diagnosis. The mean period of follow-up was 53 months. None of the patients developed congestive heart failure. We evaluated the electrocardiographic changes during the follow-up, and their association with echocardiographic findings.Results:Of the 21 patients, 12 showed one or more abnormalities on the electrocardiogram at presentation, with five demonstrating right or left ventricular hypertrophy. In all of these five cases, the tumours were mainly located in the respective ventricular cavity. In one patient with a giant tumour expanding exteriorly, there was marked left ventricular hypertrophy on the electrocardiogram. Followup studies showed spontaneous regression of the tumours in 12 of 19 patients, with abnormalities still present in only 7 patients. A gradual disappearance of left ventricular hypertrophy as seen on the electrocardiogram was noted in the patient with marked left ventricular hypertrophy at presentation in parallel with regression of the tumour.Conclusions:The presence of cardiac rhabdomyomas in patients with tuberous sclerosis might explain the ventricular hypertrophy seen on the electrocardiogram through its electrically active tissue without ventricular pressure overload or ventricular enlargement, although pre-excitation might affect the amplitude of the QRS complex. Even in cases with large tumours, nonetheless, the electric potential might not alter the surface electrocardiogram if the direction of growth of the tumour is towards the ventricular cavity. In many cases, electrocardiographic abnormalities tend to disappear, concomitant with regression of the tumours.

scholarly journals P1386 A change in left ventricular global longitudinal strain is a prognostic indicator in congestive heart failure patients with preserved ejection fraction

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
E Sakaguchi ◽  
A Yamada ◽  
M Hoshino ◽  
K Takada ◽  
N Hoshino ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Ejection Fraction ◽  
Longitudinal Strain ◽  
Global Longitudinal Strain ◽  
Stable Condition ◽  
Left Ventricular ◽  
Operating Characteristics ◽  
Cardiac Events

Abstract Purposes We examined how changes in left ventricular (LV) global longitudinal strain (GLS) were associated with prognosis in patients with preserved LV ejection fraction (LVEF) after congestive heart failure (HF) admission. Methods We studied 123 consecutive patients (age 70 ± 15 years, 55% male) who had been hospitalized due to congestive HF with preserved LVEF (> 50%). The exclusion criteria were atrial fibrillation and inadequate echo image quality for strain analyses. The patients underwent speckle-tracking echocardiography and measurement of plasma NT-ProBNP levels on the same day at the time of hospital admission as well as in the stable condition after discharge. Differences in GLS, LVEF and NT-ProBNP (delta GLS, LVEF and NT-ProBNP ; 2nd – 1st measurements) were calculated. The study end points were all-cause mortality and cardiac events. Results Mean periods of echo performance after hospitalization were 2 ±１days (1st echo) and 240 ± 289 days (2nd echo), respectively. During the follow-up (974 ± 626 days), 12 patients died and 25 patients were hospitalized because of HF worsening. In multivariate analysis, delta GLS and follow-up GLS were prognostic factors, whereas baseline and follow-up LVEF, NT-ProBNP, changes in LVEF and NT-ProBNP could not predict cardiac events. Delta GLS (p = 0.002) turned out to be the best independent prognosticator. Receiver operating characteristics analysis revealed that -0.6% of delta GLS was the optimal cut-off value to predict cardiac events and mortality (sensitivity 76%, specificity 67%, AUC 0.75). Kaplan-Meier analysis showed that patients with delta GLS more than -0.6% experienced significantly less cardiac events during the follow-up period (p < 0.0001, log-rank). Conclusion A change in LV GLS after congestive HF admission was a predictor of the prognosis in patients with preserved LVEF. It would be useful to check the changes in GLS in those with preserved LVEF after discharge.

Increased Excretion of Aldosterone in Urine From Dogs With Right-Sided Congestive Heart Failure and From Dogs With Thoracic Inferior Vena Cava Constriction

1956 ◽  
Vol 187 (1) ◽  
pp. 45-50 ◽  
Author(s):  
James O. Davis ◽  
M. Jay Goodkind ◽  
Maurice M. Pechet ◽  
Wilmot C. Ball
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Inferior Vena Cava ◽  
Cardiac Failure ◽  
Inferior Vena ◽  
Vena Cava ◽  
Bilateral Adrenalectomy ◽  
Chromatographic Fractionation

Extracts of urine from 11 normal dogs, 9 dogs with cardiac failure and 10 dogs with thoracic inferior vena cava constriction and ascites were assayed for aldosterone-like activity. The activity in urine from dogs with heart failure and from dogs with thoracic caval constriction was equivalent to 52 and 167 µg/day of DCA, respectively, and renal Na excretion was uniformly low. No activity was detected in 4 days' urine from normal dogs but chromatographic fractionation and assay of a 26-day collection of normal dog urine showed Na-retaining and increased K-excreting activity in the aldosterone fraction only. Following bilateral adrenalectomy and discontinuation of DCA therapy in 2 dogs with caval constriction, all urinary aldosterone-like activity disappeared and a natriuresis occurred. Assays of chromatographic fractions of extracts of urine from dogs with heart failure and from dogs with caval constriction revealed activity only in the aldosterone fraction.

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