Dataset Information

Association of Time Between Left Ventricular and Aortic Systolic Pressure Peaks With Severity of Aortic Stenosis and Calcification of Aortic Valve.

ABSTRACT:

Importance

Diagnosis of low-gradient severe aortic stenosis (AS) is challenging. We hypothesized that the time between left ventricular (LV) and aortic systolic pressure peaks (TLV-Ao) is associated with aortic stenosis (AS) severity and may have additive value in diagnosing severe AS, especially in patients with low-gradient AS.

Objective

To investigate the diagnostic utility of measuring catheter-based TLV-Ao in patients with severe AS.

Design, setting, and participants

We studied 123 patients with severe AS at the Cleveland Clinic Foundation, a tertiary referral center, who underwent transcatheter aortic valve replacement (TAVR) via femoral access and had pre-TAVR cardiac computed tomography assessment and hemodynamic measurements recorded during a TAVR procedure. All patients received hemodynamic evaluation, echocardiographic assessment, and quantification of aortic valve calcification (AVC) by multidetector computed tomography. Hemodynamic data were collected via left heart catheterization done just before TAVR, and TLV-Ao was calculated offline. Data were analyzed between October 5, 2015, and July 20, 2016.

Main outcomes and measures

The association between TLV-Ao and AVC or other conventional imaging parameters was analyzed.

Results

Of the included patients, the mean (SD) age was 81 (9) years, and 65 (54%) were men (54%). Among 123 patients, 48 patients (39%) had low-gradient AS (<40 mm Hg) and mean (SD) TLV-Ao was 69 (39) milliseconds. In multivariable logistic regression analyses, higher TLV-Ao (odds ratio [OR], 1.02; 95% CI, 1.01-1.04; P = .002) and higher peak aortic valve (AV) velocity (OR, 1.01; 95% CI, 1.00-1.02; P = .008) were independently associated with severe AVC (AVC >1000 AU). Adding TLV-Ao to the peak AV velocity and AV area showed significant incremental value to be associated with AVC, with a net reclassification improvement of 0.61 (95% CI, 0.23-0.99; P = .002) and integrated discriminatory improvement of 0.09 (95% CI, 0.03-0.16; P = .003). In a subgroup of patients with low-grade AS, higher TLV-Ao was the only parameter associated with severe AVC (OR, 1.02; 95% CI, 1.001-1.04; P = .03).

Conclusions and relevance

Prolonged TLV-Ao was associated with severe AVC. This catheter-based hemodynamic index may be an additional surrogate to differentiate low-gradient true severe AS. Larger, prospective studies investigating the role of TLV-Ao as a marker of clinical outcomes in patients undergoing TAVR are required.

SUBMITTER: Sato K

PROVIDER: S-EPMC6495352 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Aortic valve stenosis is the most common cardiac valve disease, and with current trends in the population demographics, its prevalence is likely to rise, thus posing a major health and economic burden facing the worldwide societies. Over the past decade, it has become more than clear that our traditional genetic views do not sufficiently explain the well-known link between AS, proatherogenic risk factors, flow-induced mechanical forces, and disease-prone environmental influences. Recent breakthroughs in the field of epigenetics offer us a new perspective on gene regulation, which has broadened our perspective on etiology of aortic stenosis and other aortic valve diseases. Since all known epigenetic marks are potentially reversible this perspective is especially exciting given the potential for development of successful and non-invasive therapeutic intervention and reprogramming of cells at the epigenetic level even in the early stages of disease progression. This review will examine the known relationships between four major epigenetic mechanisms: DNA methylation, posttranslational histone modification, ATP-dependent chromatin remodeling, and non-coding regulatory RNAs, and initiation and progression of AS. Numerous profiling and functional studies indicate that they could contribute to endothelial dysfunctions, disease-prone activation of monocyte-macrophage and circulatory osteoprogenitor cells and activation and osteogenic transdifferentiation of aortic valve interstitial cells, thus leading to valvular inflammation, fibrosis, and calcification, and to pressure overload-induced maladaptive myocardial remodeling and left ventricular hypertrophy. This is especcialy the case for small non-coding microRNAs but was also, although in a smaller scale, convincingly demonstrated for other members of cellular epigenome landscape. Equally important, and clinically most relevant, the reported data indicate that epigenetic marks, particularly certain microRNA signatures, could represent useful non-invasive biomarkers that reflect the disease progression and patients prognosis for recovery after the valve replacement surgery.