Left Ventricular Mass Regression after Two Alternative Sutureless Aortic Bioprostheses

Author(s):  
Giovanni Concistrè ◽  
Francesca Chiaramonti ◽  
Giuseppe Santarpino ◽  
Steffen Pfeiffer ◽  
Federica Marchi ◽  
...  

Objective Left ventricular (LV) hypertrophy in aortic stenosis (AS) constitutes a risk factor for cardiac morbidity and mortality. The aim of this study was to investigate the degree of LV mass regression after aortic valve replacement (AVR) with two alternative sutureless self-expanding strategies: Perceval S (Sorin Group, Saluggia, Italy) (P) and 3f Enable (Medtronic, ATS Medical, Minneapolis, MN USA) (e) aortic bioprostheses. Methods Between March 2010 and December 2011, 129 patients with symptomatic AS underwent AVR with the Perceval S or 3f Enable bioprostheses in two cardiac surgery departments (Massa, Italy; Nuremberg, Germany). We analyzed 45 patients in group P and 19 in group E undergoing isolated AVR with a 6-month follow-up. The LV mass was calculated using the Devereux formula and was indexed to body surface area. Results Baseline patient characteristics showed no significant differences between the two groups. There were no in-hospital deaths. Two patients in group P died at follow-up versus zero in group E ( P = 0.49). Mean LV mass index decreased from 146.6 (78) g/m2 at baseline to 123.3 (63) g/m2 at follow-up ( P < 0.001) in group P and from 146.1 (47.6) g/m2 to 118.1 (39.8) g/m2 ( P = 0.003) in group E, with no significant difference between the two groups ( P = 0.315). This effect was accompanied by significant clinical improvement. Conclusions: In isolated AS, AVR with sutureless bioprostheses is associated with a significant regression in LV mass at 6-month follow-up. No significant differences were present between the two alternative sutureless strategies. However, regression needs an evaluation with long-term echocardiographic examinations.

2018 ◽  
Vol 46 (9) ◽  
pp. 3959-3969 ◽  
Author(s):  
Zichuan Zhang ◽  
Peize Wang ◽  
Fei Guo ◽  
Xinmin Liu ◽  
Taiyang Luo ◽  
...  

Objective This study was performed to assess the prevalence of nonalcoholic fatty liver (NAFL) in patients with symptomatic congestive heart failure (CHF) and compare the clinical features with those of patients without NAFL. Methods In total, 102 patients with CHF were divided into NAFL and non-NAFL groups according to their hepatic ultrasonography findings. All patients underwent transthoracic echocardiography and cardiac magnetic resonance examination. Follow-up was performed for major cardiovascular events (MACE) and readmission due to heart failure at 1, 3, 6, and 12 months after the index hospitalization. Results NAFL was detected in 37 of 102 patients (36.27%). Compared with the non-NAFL group, patients with NAFL were younger, had a higher body mass index and left ventricular (LV) mass index, and had more severe fibrosis. MACE and readmission occurred in 15 patients in the NAFL group and 29 patients in the non-NAFL group, without a significant difference. Linear regression analysis revealed that after adjusting for confounders, NAFL was independently associated with the LV fibrosis size and the ratio of the LV fibrosis size to the LV mass index. Conclusions NAFL is present in more than one-third of patients with CHF and is associated with the severity of LV fibrosis.


Author(s):  
Vidhu Anand ◽  
Garvan C Kane ◽  
Christopher G Scott ◽  
Sorin V Pislaru ◽  
Rosalyn O Adigun ◽  
...  

Abstract Aims  Cardiac power is a measure of cardiac performance that incorporates both pressure and flow components. Prior studies have shown that cardiac power predicts outcomes in patients with reduced left ventricular (LV) ejection fraction (EF). We sought to evaluate the prognostic significance of peak exercise cardiac power and power reserve in patients with normal EF. Methods and results  We performed a retrospective analysis in 24 885 patients (age 59 ± 13 years, 45% females) with EF ≥50% and no significant valve disease or right ventricular dysfunction, undergoing exercise stress echocardiography between 2004 and 2018. Cardiac power and power reserve (developed power with stress) were normalized to LV mass and expressed in W/100 g of LV myocardium. Endpoints at follow-up were all-cause mortality and diagnosis of heart failure (HF). Patients in the higher quartiles of power/mass (rest, peak stress, and power reserve) were younger and had higher peak blood pressure and heart rate, lower LV mass, and lower prevalence of comorbidities. During follow-up [median 3.9 (0.6–8.3) years], 929 patients died. After adjusting for age, sex, metabolic equivalents (METs) achieved, ischaemia/infarction on stress test results, medication, and comorbidities, peak stress power/mass was independently associated with mortality [adjusted hazard ratio (HR), highest vs. lowest quartile, 0.5, 95% confidence interval (CI) 0.4–0.6, P &lt; 0.001] and HF at follow-up [adjusted HR, highest vs. lowest quartile, 0.4, 95% CI (0.3, 0.5), P &lt; 0.001]. Power reserve showed similar results. Conclusion  The assessment of cardiac power during exercise stress echocardiography in patients with normal EF provides valuable prognostic information, in addition to stress test findings on inducible myocardial ischaemia and exercise capacity.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Batzner ◽  
D Aicha ◽  
H Seggewiss

Abstract Introduction Alcohol septal ablation (PTSMA) was introduced as interventional alternative to surgical myectomy for symptomatic patients with hypertrophic obstructive cardiomyopathy (HOCM) 25 years ago. As gender differences in diagnosis and treatment of HOCM are still unclear we analyzed baseline characteristics and results of PTSMA in a large single center cohort with respect to gender. Methods and results Between 05/2000 and 06/2017 first PTSMA in our center was performed in 952 patients with symptomatic HOCM. We treated less 388 (40.8%) women and 564 (59.2%) men. All patients underwent clinical follow-up. At the time of the intervention women were older (61.2±14.9 vs. 51.9±13.7 years; p&lt;0.0001) and suffered more often from NYHA grade III/IV dyspnea (80.9% vs. 68.1%; p&lt;0.0001), whereas angina pectoris was comparable in women (62.4%) and men (59.9%). Echocardiographic baseline gradients were comparable in women (rest 65.0±38.1 mmHg and Valsalva 106.2±45.7 mmHg) and men (rest 63.1±38.3 mmHg and Valsalva 103.6±42.8 mmHg). But, women had smaller diameters of the left atrium (44.3±6.9 vs. 47.2±6.5 mm; p&lt;0001), maximal septum thickness (20.4±3.9 vs. 21.4±4.5 mm; p&lt;0.01), and maximal thickness of the left ventricular posterior wall (12.7±2.8 vs. 13.5±2.9 mm; p&lt;0.0001). In women, more septal branches (1.3±0.6 vs. 1.2±0.5; p&lt;0.05) had to be tested to identify the target septal branch. The amount of injected alcohol was comparable (2.0±0, 4 in women vs. 2.1±0.4 ml in men). The maximum CK increase was lower in women (826.0±489.6 vs. 903.4±543.0 U / l; p&lt;0.05). During hospital stay one woman and one man died, each (n.s.). The frequency of total AV blocks in the cathlab showed no significant difference between women (41.5%) and men (38.3%). Furthermore, the rate of permanent pacemaker implantation during hospital stay did not differ (12.1% in women vs. 9.4% in men). Follow-up periods of all patients showed no significant difference between women (5.7±4.9 years) and men (6.2±5.0 years). Overall, 37 (9.5%) women died during this period compared to only 33 (5.9%) men (p&lt;0.05). But, cardiovascular causes of death were not significantly different between women (2.8%) and men (1.6%). Furthermore, the rates of surgical myectomy after failed PTSMA (1.3% in women vs. 2.3% in men), ICD implantation for primary prevention of sudden cardiac death according to current guidelines (4.1% in women vs. 5.9% in men) or pacemaker implantation (3.6% in women vs. 2.0% in men) showed no significant differences. Summary PTSMA in women with HOCM was performed at more advanced age with more pronounced symptoms compared to men. While there were no differences in acute outcomes, overall long-term mortality was higher in women without differences in cardiovascular mortality. Therefore, women may require more intensive diagnostic approaches in order not to miss the correct time for gradient reduction treatment. Funding Acknowledgement Type of funding source: None


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
H Maqsood ◽  
H.A Shakeel ◽  
H.F Shoukat ◽  
M.D Khan ◽  
S.A.Y Shah ◽  
...  

Abstract Introduction Hypertrophic cardiomyopathy (HCM) is characterized by left ventricular (LV) hypertrophy in the absence of pressure overload. Manifestations of the disease include heart failure associated with diastolic dysfunction and atrial and ventricular tachyarrhythmias. Pathological features of HCM include myocyte hypertrophy, interstitial fibrosis, and myocyte disarray and are mediated by angiotensin II. Purpose This study aimed to evaluate the effects of candesartan on left ventricular (LV) hypertrophy and fibrosis in patients with hypertrophic cardiomyopathy (HCM). Methods In double-blind fashion, 30 patients (6 women, 24 men; age: 55±11 years) with HCM were randomly assigned to receive placebo (n=13) or candesartan 50 mg twice a day (n=17) for 1 year. To measure LV mass and extent of fibrosis, cardiac magnetic resonance imaging was performed at baseline and 1 year as assessed by late gadolinium enhancement. Results There was a trend toward a significant difference in the percent change in LV mass (median: +5% with placebo vs. −5% with candesartan; p=0.06). There was a significant difference in the percent change in the extent of late gadolinium enhancement, with the placebo group experiencing a larger increase (+30±27% with placebo vs. −22±44% with candesartan; p=0.03). Conclusion Our study concludes reduction of the progression of myocardial hypertrophy and fibrosis with candesartan in patients with hypertrophic cardiomyopathy. Our study population was limited so we warrant larger trials to confirm a place for angiotensin receptor blockers in the management of patients with hypertrophic cardiomyopathy. Figure 1 Funding Acknowledgement Type of funding source: Other. Main funding source(s): Self funding


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Triantafyllou ◽  
R Monteiro ◽  
A Protonotarios ◽  
T Gossios ◽  
P Elliott ◽  
...  

Abstract Introduction Early detection of affected family relatives of patients with dilated cardiomyopathy (DCM) is essential in order to guide follow up, outcomes and initiate early treatment. Myocardial work analysis is a novel method which integrated strain imaging and blood pressure and has the potential to identify patients with subclinical disease. Purpose We analysed myocardial work in family relatives of DCM patients with positive genotype but negative phenotype in order to identify whether myocardial work can identify early changes. Methods Seventy-four family relatives of DCM patients attending for screening were examined. All individuals were asymptomatic with either positive (45/74, G+) or negative (29/74, G-) genotype and no echocardiographic evidence of left ventricular dilatation or systolic impairment. Non-invasive myocardial work analysis using two-dimensional (2D) speckle tracking echocardiography was analysed. Global longitudinal strain (GLS) was measured by the same vendor specific software used for myocardial work analysis. Left ventricular (LV) ejection fraction (EF) was measured with the Simpson's biplane method. The peak systolic arm cuff blood pressure (BP) measurement at the time of echocardiography was used for the myocardial work study. Results In total we included 74 individuals (37±15 years old, 50.7% women) with mean systolic and diastolic BP of 121.3±14 and 73.2±10 mmHg respectively, mean EF was 58±5% and mean GLS at 18.4±2.5%. G+ individuals had pathogenic and very likely pathogenic mutations in 8 different genes (TTN, BAG3, DSP, FLNC, LMNA, DMD, RBM20, TPM1). There was no difference in age, systemic hypertension, diabetes or medical treatment between the 2 groups. No significant difference was found among G+ and G- individuals in mean systolic and diastolic BP (121.2±14.7 vs 121.2±15.2 mmHg), mean EF (57.3±5 vs 59.1±4%), GLS (−18.2±1.5 vs −18.6±2.9%), mean global work index (1818±403 vs 1928±295 mmHg%) and global constructive work (2192±464 vs 2260±318 mmHg%). However, we found significant reduction of the global work efficiency (GWE) with a GWE of 94.4±2.7% in the G+ versus 95.9±1.6% in the G- individuals (p 0.02). Moreover, the global wasted work (GWW) was increased in the G+ with a GWW of 111±58 mmHg% versus 82±41 mmHg% in the G- individuals (p 0.03). Conclusion DCM gene carriers show, early on, decreased myocardial work efficiency and increased wasted work compared to unaffected family members, which appears to be earlier than other parameters such as EF and GLS. Myocardial work analysis could potentially recognize individuals showing early cardiac involvement and guide closer follow up and early initiation of treatment. Funding Acknowledgement Type of funding source: None


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Pankaj Garg ◽  
Hosamadin Assadi ◽  
Rachel Jones ◽  
Wei Bin Chan ◽  
Peter Metherall ◽  
...  

AbstractCardiac magnetic resonance (CMR) is emerging as an important tool in the assessment of heart failure with preserved ejection fraction (HFpEF). This study sought to investigate the prognostic value of multiparametric CMR, including left and right heart volumetric assessment, native T1-mapping and LGE in HFpEF. In this retrospective study, we identified patients with HFpEF who have undergone CMR. CMR protocol included: cines, native T1-mapping and late gadolinium enhancement (LGE). The mean follow-up period was 3.2 ± 2.4 years. We identified 86 patients with HFpEF who had CMR. Of the 86 patients (85% hypertensive; 61% males; 14% cardiac amyloidosis), 27 (31%) patients died during the follow up period. From all the CMR metrics, LV mass (area under curve [AUC] 0.66, SE 0.07, 95% CI 0.54–0.76, p = 0.02), LGE fibrosis (AUC 0.59, SE 0.15, 95% CI 0.41–0.75, p = 0.03) and native T1-values (AUC 0.76, SE 0.09, 95% CI 0.58–0.88, p < 0.01) were the strongest predictors of all-cause mortality. The optimum thresholds for these were: LV mass > 133.24 g (hazard ratio [HR] 1.58, 95% CI 1.1–2.2, p < 0.01); LGE-fibrosis > 34.86% (HR 1.77, 95% CI 1.1–2.8, p = 0.01) and native T1 > 1056.42 ms (HR 2.36, 95% CI 0.9–6.4, p = 0.07). In multivariate cox regression, CMR score model comprising these three variables independently predicted mortality in HFpEF when compared to NTproBNP (HR 4 vs HR 1.65). In non-amyloid HFpEF cases, only native T1 > 1056.42 ms demonstrated higher mortality (AUC 0.833, p < 0.01). In patients with HFpEF, multiparametric CMR aids prognostication. Our results show that left ventricular fibrosis and hypertrophy quantified by CMR are associated with all-cause mortality in patients with HFpEF.


Medicina ◽  
2021 ◽  
Vol 57 (8) ◽  
pp. 747
Author(s):  
Rafal Berger ◽  
Hasan Hamdoun ◽  
Rodrigo Sandoval Boburg ◽  
Medhat Radwan ◽  
Metesh Acharya ◽  
...  

Background and Objectives: Over the past decade, veno-arterial extracorporeal membrane oxygenation (VA-ECMO) has developed into a mainstream treatment for refractory cardiogenic shock (CS) to maximal conservative management. Successful weaning of VA-ECMO may not be possible, and bridging with further mechanical circulatory support (MCS), such as urgent implantation of a left ventricular assist device (LVAD), may represent the only means to sustain the patient haemodynamically. In the recovery phase, many survivors are not suitably prepared physically or psychologically for the novel issues encountered during daily life with an LVAD. Materials and Methods: A retrospective analysis of our institutional database between 2012 and 2019 was performed to identify patients treated with VA-ECMO for CS who underwent urgent LVAD implantation whilst on MCS. Post-cardiotomy cases were excluded. QoL was assessed prospectively during a routine follow-up visit using the EuroQol-5 dimensions-5 level (EQ-5D-5L) and the Patient Health Questionnaire (PHQ-9) surveys. Results: Among 126 in-hospital survivors of VA-ECMO therapy due to cardiogenic shock without prior cardiac surgery, 31 (24.6%) urgent LVAD recipients were identified. In 11 (36.7%) cases, cardiopulmonary resuscitation (CPR) was performed (median 10, range 1–60 min) before initiation of VA-ECMO, and in 5 (16.7%) cases, MCS was established under CPR. Mean age at LVAD implantation was 51.7 (+/−14) years and surgery was performed after a mean 12.1 (+/−8) days of VA-ECMO support. During follow-up of 46.9 (+/−25.5) months, there were 10 deaths after 20.4 (+/−12.1) months of LVAD support. Analysis of QoL questionnaires returned a mean EQ-5D-5L score of 66% (+/−21) of societal valuation for Germany and a mean PHQ-9 score of 5.7 (+/−5) corresponding to mild depression severity. When compared with 49 elective LVAD recipients without prior VA-ECMO therapy, there was no significant difference in QoL results. Conclusions: Patients requiring urgent LVAD implantation under VA-ECMO support due to CS are associated with comparable quality of life without a significant difference from elective LVAD recipients. Close follow-up is required to oversee patient rehabilitation after successful initial treatment.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Daniel H Katz ◽  
Usman A Tahir ◽  
Debby Ngo ◽  
Mark Benson ◽  
Yan Gao ◽  
...  

Background: Increased left ventricular (LV) mass is associated with future adverse cardiovascular events including heart failure (HF). Both increased LV mass and HF disproportionately affect black individuals. To understand the mechanisms that drive disease, particularly in black individuals, we undertook a proteomic screen in a black cohort and compared it to a white cohort. Methods: We measured 1305 plasma proteins using an aptamer-based proteomic platform (SOMAscan™) in 1772 black participants in the Jackson Heart Study (JHS) with available baseline LV mass as assessed by 2D echocardiography, as well as 1600 free of HF with follow-up assessment of incident cases. Mean follow-up time was 11 years; 152 cases of incident HF hospitalization were identified. Models were adjusted for age, sex, body mass index, estimated glomerular filtration rate (as calculated by CKD-EPI equation), systolic blood pressure, hypertension treatment, presence of diabetes, total/HDL cholesterol, prevalent coronary disease, and current smoking status. Incident HF models were also adjusted for incident coronary heart disease. We then compared protein associations in JHS to those observed in whites from the Framingham Heart Study (FHS) to examine significant differences. Results: In JHS, there were 112 proteins associated with LV mass and 10 proteins associated with incident HF hospitalization with FDR <5%. Several proteins showed expected associations with both LV mass and HF, including N-terminal pro-BNP (β = 0.04 [0.02, 0.05], p = 1.0 x 10 -8 , HR = 1.46 [1.20, 1.79], p = 0.0002). The strongest association with LV mass was more novel: leukotriene A4 hydrolase (LKHA4) (β = 0.05 [0.04, 0.06], p = 2.6 x 10 -15 ). Conversely, Fractalkine/CX3CL1 showed a novel association with incident HF (HR = 1.32 [1.14, 1.54], p = 0.0003). While proteins like Cystatin C and N-terminal pro-BNP showed consistent effects in FHS, LKHA4 and Fractalkine were significantly different. Conclusions: We identify several novel biological pathways specific to black individuals hypothesized to contribute to the pathophysiologic cascade of LV hypertrophy and incident HF including LKHA4 and Fractalkine. Further studies are needed to validate these results and elucidate the detailed underlying mechanisms.


2004 ◽  
Vol 106 (3) ◽  
pp. 337-343 ◽  
Author(s):  
Leila M. M. PEREIRA ◽  
Daniele G. BEZERRA ◽  
Denise L. MACHADO ◽  
Carlos A. MANDARIM-DE-LACERDA

Stereological structural alterations of the heart and kidney were studied in four groups (n=5) of spontaneously hypertensive rats (SHRs) treated for 30 days: (i) control, (ii) NG-nitro-L-arginine methyl ester [L-NAME; nitric oxide (NO) synthesis inhibitor] alone, (iii) enalapril alone and (iv) L-NAME plus enalapril. Blood pressure (BP) was elevated significantly in NO-deficient SHRs (rats receiving L-NAME) or significantly lower in enalapril-treated SHRs. Co-administration of L-NAME and enalapril caused a 20% decrease in BP compared with untreated SHRs. NO-deficient SHRs had a decrease in body mass, but this loss of body mass was prevented efficiently in the enalapril-treated group. Enalapril treatment decreased the left ventricular (LV) mass index in SHRs, even in animals with NO synthesis blocked. NO deficiency in SHRs caused a larger decrease in the number of LV cardiomyocyte nuclei, which had a negative correlation with both LV mass index and BP. The volume-weighted glomerular volume (VWGV) separated the SHRs into two groupings: (i) control and NO-deficient SHRs, and (ii) enalapril- and L-NAME plus enalapril-treated SHRs. There was a significant difference between these two groupings, with VWGV being more than 15% smaller in the latter compared with the former grouping. The present findings reinforce the evidence that enalapril efficiently treats genetic hypertension, and demonstrate that this effect is observed even when NO synthesis is inhibited. Enalapril administration also decreases cardiac and renal structural damage caused by genetic hypertension, as well as by the interaction between genetic hypertension and NO deficiency.


2001 ◽  
Vol 12 (12) ◽  
pp. 2759-2767 ◽  
Author(s):  
Gérard M. London ◽  
Bruno Pannier ◽  
Alain P. Guerin ◽  
Jacques Blacher ◽  
Sylvain J. Marchais ◽  
...  

ABSTRACT. Left ventricular (LV) hypertrophy (LVH) is a risk factor for mortality in patients with end-stage renal disease (ESRD). Whether the attenuation of LVH has a positive effect on survival of patients with ESRD has not been documented. The aim of this study was to determine the effect of parallel treatment of hypertension and anemia on LV mass (LVM) and to determine the effect of LVM changes on survival. A cohort of 153 patients receiving hemodialysis was studied. The duration of follow-up was 54 ± 37 mo. All patients had echocardiographic determination of LV dimensions and LVM at baseline and regular intervals until the end of the follow-up period. During the study, BP decreased from (mean ± SD) 169.4 ± 29.7/90.2 ± 15.6 to 146.7 ± 29/78 ± 14.1 mmHg (P< 0.001), and hemoglobin increased from 8.65 ± 1.65 to 10.5 ± 1.45 g/dl (P< 0.001). The LV end-diastolic diameter and mean wall thickness decreased from 56.6 ± 6.5 to 54.8 ± 6.5 mm (P< 0.001), and from 10.4 ± 1.6 to 10.2 ± 1.6 mm (P< 0.05), respectively. The LVM decreased from 290 ± 80 to 264 ± 86 g (P< 0.01). Fifty-eight deaths occurred, 38 attributed to cardiovascular (CV) disease and 20 attributed to non-CV causes. According to Cox analyses after adjustment for age, gender, diabetes, history of CV disease, and all nonspecific CV risk factors, LVM regression positively affected the survival. The hazard risk ratio associated with a 10% LVM decrease was 0.78 (95% confidence interval, 0.63 to 0.92) for all-causes mortality and 0.72 (95% confidence interval, 0.51 to 0.90) for mortality due to CV disease. These results show that a partial LVH regression in patients with ESRD had a favorable and independent effect on patients’ all-cause and CV survival.


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