From Left Ventricular Hypertrophy to Congestive Heart Failure: Management of Hypertensive Heart Disease

2006 ◽  
Vol 48 (5) ◽  
pp. 326-341 ◽  
Author(s):  
Alan H. Gradman ◽  
Fadi Alfayoumi
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Heart Disease ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Hypertensive Heart Disease ◽  
Left Ventricular ◽  
Heart Failure Management

scholarly journals Potential of valsartan+sacubitril therapy in hypertensive heart disease

2021 ◽  
Vol 26 (7) ◽  
pp. 4568
Author(s):  
A. G. Ovchinnikov ◽  
A. D. Gvozdeva ◽  
A. V. Potekhina ◽  
M. V. Vitsenya ◽  
F. T. Ageev
Keyword(s):  
Heart Failure ◽  
Heart Disease ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Hypertensive Heart Disease ◽  
Hypotensive Effect ◽  
Left Ventricular ◽  
Preserved Ejection Fraction ◽  
Neprilysin Inhibitor ◽  
Is Development

The course of hypertension is often complicated by left ventricular hypertrophy (or hypertensive heart disease, HHD). The main “corridor” of natural HHD is development of heart failure with preserved ejection fraction (HFpEF). With HFpEF, the bioavailability of natriuretic peptides (NP) is significantly reduced, as a result of which the activity of cGMP-PKG signaling pathway, which plays a key role in maintaining normal diastolic function, weakens. It is possible to increase the activity of this pathway using the neprilysin inhibitor sacubitril. In case of HFpEF, the greatest efficacy from valsartan+sacubitril therapy should be expected in patients with severe concentric LVH, who have the most pronounced natriuretic peptide deficiency. Valsartan+sacubitril therapy has a clear hypotensive effect, causes a reversal of left ventricular hypertrophy and fibrosis. Since no effective treatment has yet been found for HFpEF, the main way for HHD treatment should be to prevent the diastolic dysfunction progression, which justifies valsartan+sacubitril therapy starting from the early/ asymptomatic stages.

Methods for detection of left ventricular hypertrophy: Application to hypertensive heart disease

1993 ◽  
Vol 14 (suppl D) ◽  
pp. 8-15 ◽  
Author(s):  
R. B. Devereux ◽  
M. J. Koren ◽  
G. de Simone ◽  
P. M. Okin ◽  
P. Kligfield
Keyword(s):  
Heart Disease ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Hypertensive Heart Disease ◽  
Left Ventricular

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

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