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 HUBUNGAN HIPERURISEMIA DENGAN KARDIOMEGALI PADA PASIEN GAGAL JANTUNG KONGESTIF

e-CliniC ◽  
2016 ◽  
Vol 4 (1) ◽  
Author(s):  
Keishi G. D. Masengi ◽  
Jeffrey Ongkowijaya ◽  
Frans Wantania
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Necrosis Factor Alpha ◽  
Brain Center ◽  
Factor Alpha ◽  
Cardio Vascular ◽  
Necrosis Factor

Abstract: Hyperuricemia leads to left ventricular hypertrophy that affects the occurrence of congestive heart failure. Increased uric acid level causes increased production of reactive oxygen species (ROS). This ROS stimulates tumor necrosis factor-alpha (TNF-α) which binds to tumor necrosis factor receptor (TNFR) in the heart, causing a series of reactions of myocyte apoptosis and fibrosis with left ventricular hypertrophy as the final result. This study aimed to determine the relationship between hyperuricemia and cardiomegaly in patients with congestive heart failure. This was an analytical study with a cross sectional design. Samples were 30 patients with congestive heart failure hospitalized in Irina F and Cardio Vascular Brain Center Prof. Dr. R. D. Kandou Hospital in Manado. The result of independent T test stated that there was a significant association between hyperuricemia and cardiomegaly in patients with congestive heart failure with a p value 0,020 and an odds ratio of 3.571.Keywords: hyperuricemia, cardiomegaly, left ventricular hypertrophy, congestive heart failure Abstrak: Hiperurisemia menyebabkan terjadinya hipertrofi ventrikel kiri sehingga berdampak terjadinya gagal jantung kongestif. Peningkatan kadar asam urat menyebabkan peningkatan produksi reactive oxygen species (ROS). ROS akan menstimulasi tumour necrosis factor-alpha (TNF-α) yangs selanjutnya akan berikatan dengan tumour necrosis factor receptor (TNFR) di jantung sehingga menyebabkan serangkaian reaksi apoptosis miosit dan fibrosis dengan hasil akhir hipertrofi ventrikel kiri. Penelitian ini bertujuan untuk mengetahui hubungan hiperurisemia dengan kardiomegali pada pasien gagal jantung kongestif. Penelitian ini menggunakan metode analitik dengan desain potong lintang. Sampel penelitian ini ialah 30 pasien gagal jantung kongestif di rawat inap Irina F dan Cardio Vascular Brain Center RSUP Prof. Dr. R. D. Kandou Manado. Hasil Uji T Independent menyatakan bahwa ada hubungan bermakna antara hiperurisemia dan kardiomegali pada pasien gagal jantung kongestif (p=0,020), dengan nilai odds ratio sebesar 3,571.Kata kunci: hiperurisemia, kardiomegali, hipertrofi ventrikel kiri, gagal jantung kongestif

Abstract 2180: Relationship of Left Ventricular Systolic Function to Persistence or Development of Electrocardiographic Left Ventricular Hypertrophy in Hypertensive Patients: Implications for the Development of New Heart Failure

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Peter M Okin ◽  
Kristian Wachtell ◽  
Eva Gerdts ◽  
Kurt Boman ◽  
Markku S Nieminen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Diastolic Pressure ◽  
Systolic Function ◽  
Left Ventricular ◽  
Lv Function ◽  
Increased Risk ◽  
Cornell Product

Background : We have previously demonstrated that persistence or development of ECG left ventricular hypertrophy (LVH) by Cornell product criteria are associated with an increased risk of developing heart failure (HF) compared with regression or continued absence of LVH. We postulated that this relationship might be in part mediated via worse LV systolic function in patients with new and persistent LVH. Methods : Baseline and year-3 ECG LVH and LV midwall shortening (MWS) were examined in 725 patients in the LIFE echocardiographic substudy. MWS was measured and considered abnormal if <14.2%; stress-corrected MWS (scMWS) was considered abnormal if 2440 mm-msec. Results : Between baseline and 3 years follow-up, there was continued absence (n=260) or regression (n=167) of LVH in 427 patients and persistence (n=259) or development (n=39) of ECG LVH in 298 patients. Although there was no difference in baseline prevalence of abnormal MWS (23.4 vs 26.5%, p=0.389) or abnormal scMWS (24.6 vs 26.4%, p=0.663) between groups, after 3 years follow-up persistence or development of new LVH was associated with significantly lower mean MWS and scMWS and with higher prevalence and odds of abnormal MWS and scMWS than continued absence or regression of LVH (Table ). After controlling for differences in age, gender, race, treatment group, baseline and change from baseline to year-3 of heart rate, Sokolow-Lyon voltage, systolic and diastolic pressure and baseline severity of LVH by Cornell product, persistent or new ECG LVH remained associated with a >2-fold increased risk of abnormal MWS or scMWS at year 3. Conclusions : Persistence or development of new ECG LVH during antihypertensive therapy is associated with an increased risk of LV systolic dysfunction after 3 years of follow-up. These findings provide insight into a possible mechanism by which changes in ECG LVH are associated with changing risk of developing HF. < Midwall LV Function in Relation to Persistence or Development of ECG LVH Between Baseline and Year-3

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