Septal Hypertrophy In Patients Research Articles

Prognostic Implications of Septal Hypertrophy in Patients with Heart Failure with Mildly Reduced Ejection Fraction.

Cardiac remodeling is frequently observed in patients with heart failure (HF) and serves as an indicator of disease progression and severity. Septal hypertrophy represents an aspect of remodeling that can be easily assessed via an echocardiographic measurement of the interventricular septal end diastole (IVSd), but it has not been evaluated for its prognostic value, particularly in patients with heart failure with mildly reduced ejection fraction (HFmrEF). We retrospectively included 1881 consecutive patients hospitalized with HFmrEF (i.e., a left ventricular ejection fraction of 41-49% and signs and/or symptoms of HF) at one institution during a study period from 2016 to 2022. Septal hypertrophy, defined as an IVSd > 12 mm, was prevalent in 34% of the HFmrEF patients. Although septal hypertrophy was not associated with all-cause mortality at 30 months (median follow-up) (HR = 1.067; 95% CI: 0.898-1.267; p = 0.460), it was associated with an increased risk of hospitalization due to worsening HF at 30 months (HR = 1.303; 95% CI: 1.008-1.685; p = 0.044), which was confirmed even after multivariable adjustment (HR = 1.340; 95% CI: 1.002-1.792; p = 0.049) and propensity score matching (HR = 1.399; 95% CI: 1.002-1.951; p = 0.048). Although septal hypertrophy was not associated with the risk of all-cause mortality in patients with HFmrEF, it was identified as an independent predictor of long-term HF-related rehospitalization.

Basal septal hypertrophy in patients with hypertension: a non-invasive assessment of segmental myocardial work with left ventricular pressure-strain relations

Basal septal hypertrophy in patients with hypertension: a non-invasive assessment of segmental myocardial work with left ventricular pressure-strain relations

Asymmetric septal hypertrophy in patients with severe aortic stenosis: The usefulness of associated septal myectomy

Asymmetric septal hypertrophy frequently coexists with severe aortic stenosis and can be unmasked after successful aortic valve replacement (AVR), jeopardizing the clinical and echocardiographic results. The aim of our study was to investigate, at 5 years postoperatively, the effectiveness of myectomy associated with AVR on left ventricular (LV) mass regression and LV diastolic function. From 1997 and 2004, 86 patients with a diagnosis of severe aortic stenosis and asymmetric septal hypertrophy consecutively underwent AVR (group A) or AVR and concomitant myectomy (group B). To assess the improvement in LV mass and LV diastolic function, we studied the 52 survivors (23 in group A and 29 in group B) who had the same prosthesis type (beleaflet mechanical), the same size (21 mm), and the same follow-up length. In group A, the LV mass index regressed from 119.2 ± 22.0 to 113.8 ± 21.8, and in group B, it regressed from 121.6 ± 20.8 to 112.7 ± 20.0 (P<.0005). In group A, the E/E' ratio improved from 15.3 ± 3.0 to 11.8 ± 3.0, and in group B, it improved from 16.2 ± 3.2 to 12.1 ± 3.3 (P=.02). Surgeons should inspect the LV outflow tract at AVR. Concomitant myectomy at AVR is a safe and effective procedure that improves LV mass regression and LV diastolic function.

Asymmetric septal hypertrophy in patients with coronary artery disease

To assess the relationship between asymmetric septal hypertrophy (ASH) and manifestations of coronary artery disease (CAD). A total of 5128 consecutive patients with proven diagnosis of CAD were examined. There were 2469 patients with left ventricular (LV) hypertrophy (LVH) (48.2%), among whom 297 (5.8%) had ASH (echocardiographic ventricular septum thickness to LV posterior wall thickness ratio > or =1.3). There were more male patients with ASH than patients with symmetric LVH (SLVH). ASH patients were significantly older and more obese, more of them were in NYHA class III/IV compared with SLVH patients. The prevalence of prior myocardial infarction (MI), systemic hypertension, heart rhythm disorders were higher in patients with ASH compared with SLVH patients. The groups differed significantly in echocardiographic parameters: LV and right ventricular (RV) end-diastolic dimensions, LV ejection fraction, left atrial dimension, extent of LV wall motion abnormalities, wall motion score index, LV mass/body surface area, signs of prior MI, and frequency of moderate mitral regurgitation. The frequency of stenosis and more severe (>90% stenosis) lesion of right coronary artery (RCA) and left circumflex artery (LCA) were higher in patients with ASH. Multivariate analysis identified that heart rhythm disorder, LV and RV end-diastolic dimensions, aortic root diameter, impaired LV ejection fraction, echocardiographic signs of previous MI, LV mass, and severe lesions of RCA were independently associated with ASH. In patients with CAD, ASH is associated with significant atherosclerosis of RCA and LCA, and more severe clinical manifestations of CAD and impaired LV function.

Visualization of transcoronary ablation of septal hypertrophy in patients with hypertrophic obstructive cardiomyopathy: a comparison between cardiac MRI, invasive measurements and echocardiography

ObjectiveHypertrophic obstructive cardiomyopathy (HOCM) is treated by surgical myectomy or transcoronary ablation of septal hypertrophy (TASH). The aim of this study was to visualize the feasibility, success and short-term results of TASH on the basis of cardiac MRI (CMR) in comparison with cardiac catheterization and echocardiography.MethodsIn this in vivo study, nine patients with HOCM were treated with TASH. Patients were evaluated by transthoracic echocardiography, invasive cardiac angiography and CMR. Follow-up examinations were carried out after 1, 3 and 12 months. MR imaging was performed on a 1.5-T scanner. All images were processed using the semiautomatic Argus software and were evaluated by an attending thoracic radiologist and cardiologist.ResultsThe echocardiographic pressure gradient (at rest) was 69.3 ± 15.3 mmHg before and 22.1 ± 5.7 mmHg after TASH (P < 0.01, n = 9). The flux acceleration over the aortic valve examined (V max) was 5.1 ± 0.6 m/s before and 3.4 ± 0.3 m/s after the TASH procedure (P < 0.05). Also, there was a decrease of septum thickness from 22.0 ± 1.2 to 20.2 ± 1.0 mm (P < 0.05) after 6 ± 3 weeks. The invasively assessed pressure gradient at rest was reduced from 63.7 ± 15.2 to 21.2 ± 11.1 mmHg (P < 0.01) and the post-extrasystolic gradient was reduced from 138.9 ± 12.7 to 45.6 ± 16.5 mmHg (P < 0.01). All differences as well as the quantity of injected ethanol were plotted against the size or amount of scar tissue as assessed in the MRI. There was a statistically significant correlation between the post-extrasystolic gradient decrease and the amount of scar tissue (P = 0.03, r 2 = 0.5). In addition, the correlation between the quantity of ethanol and scar tissue area was highly significant (P < 0.01, r 2 = 0.6), whereas the values for the gradient deviation (P = 0.10, r 2 = 0.34), ΔV max (P = 0.12, r 2 = 0.31), as well as the gradient at rest (P = 0.27, r 2 = 0.17) were not significant.ConclusionTASH was consistently effective in reducing the gradient in all patients with HOCM. In contrast to the variables investigated by echocardiography, the invasively measured post-extrasystolic gradient correlated much better with the amount of scar tissue as assessed by CMR. We conclude that the optimal modality to visualize the TASH effect seems to be a combination of CMR and the invasive identification of the post-extrasystolic gradient.

Catheter Treatment for Hypertrophic Obstructive Cardiomyopathy

Hypertrophic cardiomyopathy is a relatively recent concept. It occurs not infrequently; ≈1 in 500 individuals within the general population is a carrier of the disease.1 The main genes responsible for hypertrophic cardiomyopathy have been characterized and can be determined with relative ease.2 Some patients develop subaortic obstruction. The original term, idiopathic hypertrophic subaortic stenosis, dates to 1964;3 since then, it has become obvious that the obstructive component has its own prognostic meaning. The obstruction occurs in ≈25% of all humans with hypertrophic cardiomyopathy,4 and the entity is now called hypertrophic obstructive cardiomyopathy. Article p 131 Surgery for elimination of the obstructive element via resection of the subaortic septal bulge (myectomy) has been, since its introduction by Cleland at the Brompton in London exactly half a century ago, the only rational option for patients with clinically relevant left ventricular outflow tract obstruction that is refractory to optimal medical therapy. At experienced centers, the operation can be performed with low mortality and excellent clinical improvement.5 The concept of using transluminal techniques to reduce septal hypertrophy in patients with hypertrophic obstructive cardiomyopathy was not based on the hope of achieving better results than with surgery, but primarily to reduce morbidity. In the early 1980s, while performing coronary angiography on patients with hypertrophic obstructive cardiomyopathy, I noticed that in some patients, the first septal perforator branches appeared to irrigate primarily the area of the septal bulge responsible for outflow tract obstruction. During systole, these branches seemed to be compressed by the surrounding hyperabundant myocardium. Interfering with the proper irrigation of this …

Electrophysiological Characteristics of Septal Hypertrophy in Patients With Hypertrophic Obstructive Cardiomyopathy and Moderate to Severe Symptoms

In hypertrophic obstructive cardiomyopathy, regional hypertrophy, myocardial replacement scarring, expanded interstitial fibrosis, and myocardial disarray can be found. The electrophysiological consequences of this substrate have not yet been investigated. Thus, the aim of this study was to assess the local electrophysiological characteristics of regional left ventricular (LV) septal hypertrophy. In 9 patients with hypertrophic obstructive cardiomyopathy, electroanatomic voltage mapping of the LV was performed during sinus rhythm to determine the regional voltage amplitude. In addition, the morphology of the regional bipolar endocardial electrogram was assessed. During multisite LV stimulation, the stimulus-to-V intervals in both septal hypertrophy and the lateral LV myocardium were determined. Bipolar electroanatomic voltage mapping revealed a significant reduction in regional voltage amplitude in septal hypertrophic areas compared with lateral LV areas without evidence of hypertrophy (0.41+/-0.24 versus 13.5+/-1.85 mV; P<0,001). Local bipolar electrogram analysis demonstrated fractionated and prolonged endocardial potentials in septal hypertrophic areas (with split potentials present in 6 patients) that were not revealed at lateral myocardial sites (110.1+/-24.6 versus 80.1+/-6.6 ms; P=0.005). The stimulus-to-V interval was significantly longer (62.9+/-10.3 versus 24.1+/-9.1 ms; P=0.005) in septal hypertrophic areas compared with the lateral LV. In LV regions with extensive hypertrophy, a marked reduction of bipolar voltage amplitude can be found, as well as local conduction delay and conduction block. This result is consistent with the findings of regional myocardial scarring and may contribute to the increased incidence of ventricular tachyarrhythmias in patients with hypertrophic obstructive cardiomyopathy.

Percutaneous Transluminal Septal Artery Ablation Using Polyvinyl Alcohol Foam Particles for Septal Hypertrophy in Patients With Hypertrophic Obstructive Cardiomyopathy: Acute and 3-Year Outcomes

To investigate the effect of septal artery occlusion with transluminally delivered polyvinyl alcohol (PVA) foam particles for the treatment of hypertrophic obstructive cardiomyopathy (HOCM). Percutaneous septal artery ablation was performed in 18 symptomatic patients (13 men; mean age 60+/-17 years, range 28-89) with drug-resistant HOCM. PVA foam particles were mixed with contrast medium and injected through an angiographic catheter under fluoroscopic control until complete stasis in the septal branch was achieved. Patients were monitored with echocardiography and cardiovascular magnetic resonance imaging. The septal artery was successfully occluded in all patients; no embolization of other coronary branches occurred after infusion of 3 to 8 mL (5.2+/-0.8) of PVA foam particles. The resting pressure gradient was diminished from 83+/-32 to 31+/-35 mmHg (p<0.05). Over a mean follow-up of 44+/-4 months, all patients had symptomatic improvement of their dyspnea and workload without the need for intensified drug therapy. The average NYHA functional class decreased from 3.3+/-0.5 to 1.3+/-0.7 (p<0.0001), with a significant increase in the area of the left ventricular outflow tract (1.3+/-0.2 to 2.6+/-0.2 cm2, p<0.0001). Three instances of transient atrioventricular block occurred, but no complete heart block was produced by the embolization procedure. Embolization of the septal artery with PVA foam particles appears effective and safe in this series of patients with hypertrophic obstructive cardiomyopathy. The pure ischemic infarction produced by PVA ablation might be the responsible for the lack of complete heart block and the need for permanent pacing.

Asymmetrical septal hypertrophy in patients with hypertension: a type of hypertensive left ventricular hypertrophy or hypertrophic cardiomyopathy combined with hypertension?

To determine whether asymmetrical septal hypertrophy (ASH) in patients with essential hypertension (HT) is a type of hypertensive left ventricular (LV) hypertrophy or hypertrophic cardiomyopathy (HCM) combined with HT, we investigated a group of 7 hypertensive patients with ASH compared with 12 HCM patients and 10 healthy controls using radionuclide angiography and right ventricular endomyocardial biopsy. The LV time-volume curve and its first and second derivative curves were constructed from cardiac output and time-activity curves constructed by combined forward and reverse-gating from the R wave. The LV wall thickness and ejection fraction were significantly greater in both the HT and HCM groups than in the control group, whereas there were no differences in these indices between the HT and HCM groups. Rapid filling volume index and rapid filling fraction showed significantly lower values in the HCM group than in the control group (p < 0.005). In contrast to the HCM group, these indices in the HT group did not differ from those in the control group. The time to peak filling rate was prolonged in the control, hypertension, and HCM groups in increasing order. Histopathological study revealed a higher incidence of myocardial cell disarray in the HCM than in the HT group. The above results suggest that ASH in hypertensive patients is a type of hypertensive LV hypertrophy.

Disproportionate Septal Hypertrophy Associated With Erythroblastosis Fetalis

We retrospectively reviewed clinical and echocardiographic data on 10 newborns with erythroblastosis fetalis who were admitted to our nurseries between 1984 and 1988 and who required a double-volume exchange transfusion and neonatal intensive care. Echocardiograms were performed in the first 48 hours of life. In 5 patients, disproportionate septal hypertrophy was demonstrated; 1 additional patient had biventricular hypertrophy with a thickened septum but not disproportionate septal hypertrophy. The mean septal: left ventricular free-wall ratio for the group (n = 10) was 1.37. No correlation was apparent between the occurrence of disproportionate septal hypertrophy and newborn glucose, bilirubin, or hematocrit values. When analyzed separately, the 4 patients who did not receive intrauterine blood transfusions had a ratio of 1.73 +/- 0.21 (mean +/- SEM); this was significantly greater than the ratio in the 6 patients who were transfused in utero (1.13 +/- 0.24). In patients who underwent transfusions, there was no correlation between the number of transfusions and the septal:left ventricular ratio. This study reports a significant but previously unrecognized cardiac hypertrophy with disproportionate septal hypertrophy in patients with erythroblastosis fetalis. Our data suggest a sparing effect of intrauterine fetal transfusions. The mechanism by which these transfusions may affect the hypertrophic development of the myocardium remains to be determined.

Mechanism of development of asymmetric septal hypertrophy in patients with essential systemic hypertension.

In order to understand the mechanism of development of asymmetric septal hypertrophy (ASH) in hypertension, 290 patients with essential hypertension (HT) were examined echocardiographically. Out of them 84 cases of advanced left ventricular hypertrophy (LVH) [37 cases of symmetric hypertrophy (HT-SH group) and 47 cases of ASH (HT-ASH group)] were compared in their clinical and echocardiographic findings with hypertrophic cardiomyopathy (HCM). In the 290 HT cases, the highest systolic pressure in each patient's history was found to correlate with left ventricular (LV) posterior wall thickness (PWT), but not with the septal wall thickness (IVST). There were no differences in LV thickness (IVST + PWT) among patients in the HT-ASH, HT-SH and HCM groups. While the HCM group patients showed no significant differences in IVST and PWT from those in the HT-ASH group, they did have greater IVST and smaller PWT than HT-SH group patients. The rapid filling rate (RFR) was also not much different in the HCM and HT-ASH groups, but was significantly lower in the HCM group than in the HT-SH group. Furthermore, HT-ASH group patients has a milder degree of hypertension and a higher incidence of familial occurrence of HCM than did those in the HT-SH group. After treatment for HT, the HT-SH group showed a significant decrease in wall thickness during long-term observation, while the HT-ASH and HCM groups, failed to exhibit such changes. Moreover, the degree of myocardial disarrangement in the HT-ASH group did not differ significantly from that in the HCM group. These results suggested that LVH in HT is related not only to pressure load but also to genetic factors similar to that in HCM.

Asymmetric septal hypertrophy in patients with aortic stenosis: An adaptive mechanism or a coexistence of hypertrophic cardiomyopathy

Myocardial histologic features and left ventricular dynamics were assessed in 24 patients with severe aortic stenosis, 12 with (group 1) and 12 without (group 2) associated asymmetric septal hypertrophy. In 10 patients from group 1, echocardiography showed a septal/pos-terior wall ratio of 1.5; in the other 2, asymmetric septal hypertrophy was diagnosed by direct inspection at the time of surgery. Septal myectomy in all 12 patients in group 1 was completed at the time of aortic valve replacement. Septal histologic features were assessed from surgical specimens in 10 patients in group 1. Transseptal endomyocardial biopsy specimens of the anterolateral wall taken during preoperative cardiac catheterization were evaluated by light microscopy in 10 patients from group 1 and all patients of group 2. Left ventricular end-diastolic and peak systolic pressure, peak pressure gradient, calculated valve area and angiographic muscle mass did not differ significantly in groups 1 and 2; ejection fraction (68 versus 58%; probability [p] < 0.01) was larger and end-diastolic volume (109 versus 144 ml/m 2 ; difference not significant [NS]) was smaller in group 1 than in group 2. Muscle fiber diameter of the anterolateral wall was similar in groups 1 and 2 (26.5 versus 29.1 μ; NS), but muscle fiber diameter of the septum in group 1 was significantly smaller (24.4 μ; p < 0.01) than that of the anterolateral wall in group 2. No morphologic abnormalities typical for hypertrophic cardiomyopathy (fiber disarray) were seen in samples from the patients in either group. By 18 months postoperatively, septal wall thickness had decreased significantly from 2.0 to 1.5 cm (p < 0.01) and posterior wall thickness from 1.4 to 1.2 cm (p < 0.05) in group 1. In group 2, septal wall thickness decreased from 1.5 to 1.3 cm (NS) and posterior wall thickness from 1.4 to 1.2 cm (NS) 8 months postoperatively. Asymmetric septal hypertrophy in patients with aortic stenosis is an adaptive mechanism to the long-standing pressure overload, and hence there is no evidence of coexistence of idiopathic hypertrophic cardiomyopathy and aortic valve disease. Although the degree of valve obstruction was similar in both groups, left ventricular ejection performance was significantly lower in the group without asymmetric hypertrophy, probably because these patients had a more advanced stage of myocardial disease. After successful valve replacement, there is a significant regression of septal hypertrophy in patients with aortic stenosis and asymmetric septal hypertrophy.

Asymmetric septal hypertrophy in patients with aortic stenosis: An adaptive mechanism or a co-existence of hypertrophic cardiomyopathy?

Asymmetric septal hypertrophy in patients with aortic stenosis: An adaptive mechanism or a co-existence of hypertrophic cardiomyopathy?

Asymmetric Septal Hypertrophy in Patients on Long-Term Hemodialysis

Echocardiographic studies were performed in 23 hypertensive patients who were receiving therapy with long-term hemodialysis. Five patients (22 percent) had normal thickness of the left ventricular wall. Eleven (48 percent) had symmetric left ventricular hypertrophy, and seven (30 percent) showed asymmetric septal hypertrophy, with a ratio of septal to posterior wall thickness of 1.3 or greater. The latter group differed from patients with hypertrophic cardiomyopathy in that patients on long-term hemodialysis had a dilated left ventricular dimension, a relatively normal diastolic slope of the mitral valve, absence of systolic motion of the mitral valve, and a septal to posterior wall ratio of less than 1.5. A high incidence of asymmetric septal hypertrophy in this and other studies indicates that this condition is not specific for hypertrophic cardiomyopathy. We suggest that in addition to asymmetric septal hypertrophy, the diagnosis of hypertrophic cardiomyopathy should be made in the light of the clinical picture, as well as other echocardiographic features.