scholarly journals Non-surgical management of an acute decompensated heart failure patient with severe aortic stenosis and concomitant left ventricular outflow tract obstruction

2021 ◽  
Author(s):  
Tomoyo Hamana ◽  
Hiroyuki Yamamoto ◽  
Nobuyuki Takahashi ◽  
Hiroshi Tsunamoto ◽  
Testuari Onishi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Aortic Stenosis ◽  
Heart Failure Patient ◽  
Left Ventricular Outflow Tract ◽  
Acute Decompensated Heart Failure ◽  
Severe Aortic Stenosis ◽  
Decompensated Heart Failure ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Left Ventricular Outflow

scholarly journals INDIRECT ULTRASOUND EVALUATION OF LEFT VENTRICULAR OUTFLOW TRACT DIAMETER IMPLICATIONS FOR HEART FAILURE AND AORTIC STENOSIS SEVERITY ASSESSMENT.

2020 ◽  
Author(s):  
Gabriele Pestelli ◽  
Andrea Fiorencis ◽  
Valeria Pergola ◽  
Giovanni Luisi ◽  
Vittorio Smarrazzo ◽  
...  
Keyword(s):  
Heart Failure ◽  
Aortic Stenosis ◽  
Aortic Root ◽  
Left Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Outflow Tract ◽  
Regression Equation ◽  
Ultrasound Evaluation ◽  
Left Ventricular Outflow

Background. Whereas dependency of left ventricular outflow tract diameter (LVOTD) from body surface area (BSA) has been established and a BSA-based LVOTD formula has been derived, the relationship between LVOTD and aortic root and LV dimensions has never been explored. This may have implications for evaluation of LV output in heart failure (HF) and aortic stenosis (AS) severity. Methods. A cohort of 540 HF patients who underwent transthoracic echocardiography was divided in a derivation and validation subgroup. In the derivation subgroup (N=340) independent determinants of LVOTD were analyzed to derive a regression equation, which was used for predicting LVOTD in the validation subgroup (N=200) and compared with the BSA-derived formula. Results. LVOTD determinants in the derivation subgroup were sinuses of Valsalva diameter (SVD, beta=0.392, P<0.001), BSA (beta=0.229, P<0.001), LV end-diastolic diameter (LVEDD, beta=0.145, P=0.001), and height (beta=0.125, P=0.037). The regression equation for predicting LVOTD with the aforementioned variables (LVOTD=6.209+[0.201xSVD]+[1.802xBSA]+[0.03xLVEDD]+[0.025xHeight]) did not differ from (P=0.937) and was highly correlated with measured LVOTD (R=0.739, P<0.001) in the validation group. Repeated analysis with LV end-diastolic volume instead of LVEDD and/or accounting for gender showed similar results, whereas BSA-derived LVOTD values were different from measured LVOTD (P<0.001). Conclusion. Aortic root and LV dimensions affect LVOTD independently from anthropometric data and are included in a new comprehensive equation for predicting LVOTD. This should improve evaluation of LV output in HF and severity of AS, avoiding use of LVOT velocity-time integral alone, which can be misleading, especially when LV cavity and aortic root dimensions are abnormal.

Left ventricular outflow tract obstruction masked by severe aortic stenosis

2015 ◽  
Vol 65 (3) ◽  
pp. 160-163 ◽  
Author(s):  
Shinya Fukui ◽  
Masataka Mitsuno ◽  
Mitsuhiro Yamamura ◽  
Hiroe Tanaka ◽  
Masaaki Ryomoto ◽  
...  
Keyword(s):  
Aortic Stenosis ◽  
Left Ventricular Outflow Tract ◽  
Severe Aortic Stenosis ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Outflow Tract ◽  
Ventricular Outflow Tract Obstruction ◽  
Left Ventricular Outflow

scholarly journals Outcomes in Patients With Obstructive Hypertrophic Cardiomyopathy and Concomitant Aortic Stenosis Undergoing Surgical Myectomy and Aortic Valve Replacement

2021 ◽  
Author(s):  
Milind Y. Desai ◽  
Alaa Alashi ◽  
Zoran B. Popovic ◽  
Per Wierup ◽  
Brian P. Griffin ◽  
...  
Keyword(s):  
Risk Factors ◽  
Aortic Valve ◽  
Aortic Stenosis ◽  
Left Ventricular Outflow Tract ◽  
Severe Aortic Stenosis ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Outflow Tract ◽  
Left Ventricular Outflow ◽  
Surgical Myectomy

Background Hypertrophic cardiomyopathy (HCM) and aortic stenosis can cause obstruction to the flow of blood out of the left ventricular outflow tract into the aorta, with obstructive HCM resulting in dynamic left ventricular outflow tract obstruction and moderate or severe aortic stenosis causing fixed obstruction caused by calcific degeneration. We sought to report the characteristics and longer‐term outcomes of patients with severe obstructive HCM who also had concomitant moderate or severe aortic stenosis requiring surgical myectomy and aortic valve replacement. Methods and Results We studied 191 consecutive patients (age 67±6 years, 52% men) who underwent myectomy and aortic valve (AV) replacement (90% bioprosthesis) at our center between June 2002 and June 2018. Clinical and echo data including left ventricular outflow tract gradient and indexed AV area were recorded. The primary outcome was death. Prevalence of hypertension (63%) and hyperlipidemia (75%) were high, with a Society of Thoracic Surgeons score of 5±4, and 70% of participants had no HCM‐related sudden death risk factors. Basal septal thickness and indexed AV area were 1.9±0.4 cm and 0.72±0.2 cm 2 /m 2 , respectively, while 100% of patients had dynamic left ventricular outflow tract gradient >50 mm Hg. At 6.5±4 years, 52 (27%) patients died (1.5% in‐hospital deaths). One‐, 2‐, and 5‐year survival in the current study sample was 94%, 91%, and 83%, respectively, similar to an age‐sex–matched general US population. On multivariate Cox survival analysis, age (hazard ratio [HR], 1.65; 95% CI, 1.24–2.18), chronic kidney disease (HR, 1.58; 95% CI, 1.21–2.32), and right ventricular systolic pressure on preoperative echocardiography (HR, 1.28; 95% CI, 1.05–1.57) were associated with longer‐term mortality, but traditional HCM risk factors did not. Conclusions In symptomatic patients with severely obstructive HCM and moderate or severe aortic stenosis undergoing a combined surgical myectomy and AV replacement at our center, the observed postoperative mortality was significantly lower than the expected mortality, and the longer‐term survival was similar to a normal age‐sex–matched US population.

scholarly journals Prevalence and prognostic impact of left ventricular outflow tract calcification in patients with severe aortic stenosis undergoing transfemoral TAVI using second-generation devices

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
L Waldschmidt ◽  
A Gossling ◽  
S Ludwig ◽  
M Linder ◽  
L Voigtlaender ◽  
...  
Keyword(s):  
Aortic Stenosis ◽  
Second Generation ◽  
Left Ventricular Outflow Tract ◽  
Severe Aortic Stenosis ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Outflow Tract ◽  
All Cause Mortality ◽  
Left Ventricular Outflow ◽  
Transfemoral Tavi

Abstract Introduction Left ventricular outflow tract (LVOT) calcification is known to be associated with adverse outcomes after TAVI in patients receiving first-generation transcatheter heart valves (THV). Second-generation THV have been shown to improve outcomes of TAVI patients. Thus, aim of this study is to assess the prevalence of LVOT calcification as well as its impact on procedural and clinical outcomes in patients with severe aortic stenosis undergoing transfemoral TAVI with second-generation THV in a real-world patient cohort. Methods In this retrospective single-center analysis patients receiving transfemoral TAVI with second-generation THV for the treatment of aortic stenosis (AS) between 05/2012 and 06/2018 and with adequate CT data were included (n=836). Amount of LVOT calcification was measured quantitatively from contrast-enhanced multislice CT using a dedicated software. Baseline characteristics and outcomes were compared according to presence of significant LVOT calcification (none/≤10 mm3 vs. &gt;10 mm3). Procedural and clinical outcome were assessed in accordance with VARC-2 criteria. All-cause mortality was assessed by Kaplan-Meier method, median follow-up was 1.4 years. Results Significant LVOT calcification was present in 37.0% of patients. Patients with LVOT calcification were older (all results as follows without (w/o) vs. with (w) LVOT calcification: 81.4 (77.1, 84.8) vs. 82.3 (78.0, 86.3) years, p=0.006), but presented similar STS scores compared to those without LVOT calcification (5.4±4.7 vs. 5.4±3.5%, p=0.94). Moreover, patients with LVOT calcification had higher mean transvalvular gradients at baseline (30.0 (21.0, 41.0) vs. 37.0 (25.7, 47.0) mmHg, p&lt;0.001) and higher aortic valve calcium volume (380.7 (226.8, 632.1) vs. 663.6 (364.5, 1070.3) mm3, p&lt;0.001). There were no significant differences in rate of device success (97.0 vs. 94.2%, p=0.11), renal failure (2.6 vs. 2.3%, p=1.00), myocardial infarction (0.9 vs. 1.2%, p=1.00) or rate of permanent pacemaker implantation at 30 days after TAVI (16.6 vs. 17.2%, p=0.91). However, rate of TIA/stroke was significantly higher in patients with LVOT calcification (2.1 vs. 6.2%, p=0.0098). Furthermore, patients with LVOT calcification had a higher rate of more than mild paravalvular leakage at discharge (3.8 vs. 7.6%, p=0.033). Rate of 1 year all-cause mortality (17.8 vs. 21.2%, p=0.23) was not significantly different between both groups. Conclusions Significant LVOT calcification is present in a substantial proportion of patients receiving TAVI. In such patients, higher rates of cerebrovascular events and more than mild PVL occurred compared to those without significant LVOT calcification even with currently available second-generation THV. Although these findings did not translate into higher mortality rates in the present study, they underline the need for further optimization of THV technology in order to improve outcomes among all TAVI patients. Figure 1. 1-year mortality Funding Acknowledgement Type of funding source: None

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