Circulation Editors’ Picks

Hypertrophy is considered one of the major mechanisms of the myocardium for adapting to hemodynamic overload. More muscle mass provides more contractile elements for generating the extra work required by the overload. In pressure overload of aortic valve stenosis, concentric left ventricular hypertrophy (LVH) normalizes wall stress, a key determinant of ejection performance.1 Afterload is often expressed as wall stress (pressure×radius/thickness). As the pressure term in the numerator increases, it is offset by an increase in the thickness term of the denominator. In this way, the high systolic pressure required to drive blood through even a very stenotic aortic valve can be consistent with normal afterload and normal ejection fraction. See p 3170 Unfortunately, hypertrophy not only provides benefits but also has many pathological consequences. One of these is myocardial ischemia and the attendant angina reported by patients with aortic stenosis despite normal epicardial coronary arteries. The onset of angina greatly increases the risk of sudden death compared with the risk in asymptomatic patients with aortic valve stenosis.2,3 Angina occurs when myocardial oxygen demand exceeds supply. Demand is proportional to heart rate and wall stress, and the latter can be elevated in cases of aortic stenosis when hypertrophy is inadequate to normalize stress.1 After aortic valve replacement, there is marked regression of hypertrophy that may occur over the next several months to years,4 but angina is relieved immediately. Relief of angina immediately after surgery is probably due to the combination of sudden decreased oxygen demand after removal of pressure overload and increased oxygen supply of improved perfusion. However, there are remaining questions about the physiological mechanisms for reduced myocardial oxygen supply (coronary blood flow) in aortic stenosis and its improvement after relief of pressure overload. Specifically, what is it about critical aortic stenosis that is “critical” …

Case presentation: A 66-year-old man is referred to a cardiologist for the evaluation of a heart murmur. The patient claims to be entirely asymptomatic, although his wife notes that he has decreased his physical activity over the past two years because he is “getting old.” At physical examination, his blood pressure was 120/70 mm Hg; pulse, 80 bpm; respiration, 13 breaths per minute; and temperature, 99.0°F. Cardiovascular examination revealed normal central venous pressure. His carotid upstrokes were reduced in volume and delayed in upstroke. Cardiac examination revealed a forceful sustained apical impulse in its normal position. There was a 3/6 late-peaking systolic ejection murmur heard at the right upper sternal border radiating to the neck. The rest of the physical examination was unremarkable. Echo-Doppler evaluation revealed an ejection fraction of 0.60, a left ventricular free wall thickness of 1.3 cm, and a peak transaortic flow velocity of 4.5 m/s. How should this patient be managed? Should he undergo aortic valve replacement now? Should he undergo longitudinal follow-up to monitor progression of his aortic stenosis? Over the past 40 years, diagnostic techniques, substitute cardiac valves, and valve implantation surgery have undergone continued improvement, reducing the risk of the valve replacement and enhancing its benefits. Thus, the risk-benefit analysis of valve surgery has tilted in favor of increasingly early intervention for valve disease. The following is a summary incorporating this concept into the current strategy for managing patients with aortic stenosis such as the one described above. The patient with severe aortic stenosis who presents with symptoms represents the most straightforward management strategy for the disease. Survival is nearly normal until the classic symptoms of angina, syncope, or dyspnea develop.1 However, only 50% of patients who present with angina survive 5 years, whereas 50% survival is 3 years for patients who …

Received October 26, 2004; revision received January 13, 2005; accepted February 4, 2005. Calcific aortic valve disease is a slowly progressive disorder with a disease continuum that ranges from mild valve thickening without obstruction of blood flow, termed aortic sclerosis, to severe calcification with impaired leaflet motion, or aortic stenosis (Figure 1). In the past, this process was thought to be “degenerative” because of time-dependent wear-and-tear of the leaflets with passive calcium deposition. Now, there is compelling histopathologic and clinical data suggesting that calcific valve disease is an active disease process akin to atherosclerosis with lipoprotein deposition, chronic inflammation, and active leaflet calcification. The overlap in the clinical factors associated with calcific valve disease and atherosclerosis and the correlation between the severity of coronary artery and aortic valve calcification provide further support for a shared disease process. Figure 1. Gross specimen of minimally diseased aortic valve (left) and severely stenotic aortic valve (right). In the severely stenotic valve, there are prominent lipocalcific changes on aortic side of valve cusps (arrow), with sparing of commissures. ### Anatomy of Normal Aortic Valve The normal aortic valve comprises 3 layers. The ventricularis, on the ventricular side of the leaflet, is composed of elastin-rich fibers that are aligned in a radial direction, perpendicular to the leaflet margin. The fibrosa, on the aortic side of the leaflet, comprises primarily fibroblasts and collagen fibers arranged circumferentially, parallel to the leaflet margin. The spongiosa is a layer of loose connective tissue at the base of the leaflet, between the fibrosa and ventricularis, composed of fibroblasts, mesenchymal cells, and a mucopolysaccharide-rich matrix. These layers work in concert to provide tensile strength and pliability for decades of repetitive motion. ### Early Lesion of Aortic Sclerosis Histopathologic studies of aortic sclerosis show focal subendothelial plaquelike lesions on the aortic side of the leaflet that extend to the adjacent fibrosa layer. Similarities to …

Robotic aortic valve replacement

Role of Multimodal Cardiac Imaging in Low-Flow, Low-Gradient Aortic Stenosis

In adults with valvular aortic stenosis (AS), valve replacement is recommended in the presence of symptoms and severely reduced aortic valve area (AVA).1 In such patients, valve replacement improves symptoms and survival, even in the setting of left ventricular (LV) dysfunction. LV dysfunction in severe AS is usually due to afterload mismatch; valve replacement relieves the afterload excess imposed by the stenotic valve and improves LV performance. 2 However, a subset of patients with “ severe” AS, LV dysfunction, and low-transvalvular gradient has been reported to have a relatively high operative mortality and poor prognosis.2–4⇓⇓ This clinical scenario has been termed “low-flow, low-gradient AS.” Accurate assessment of AVA in such patients is difficult because (1) calculated AVA is directly proportional to forward stroke volume, and (2) the Gorlin constant varies at low-flow states. 5–7⇓⇓ Some patients with low-flow, low-gradient AS have a reduced AVA as a result of inadequate forward stroke volume rather than anatomic stenosis, a situation analogous to reduced anterior mitral leaflet excursion in dilated cardiomyopathy where there is not enough forward flow to fully open the valve. For example, Cannon et al 8 showed that some patients with low-gradient AS were found to have only mild AS at surgery despite a Gorlin AVA indicating critical AS. Obviously, surgical therapy is unlikely to benefit such patients because their primary pathology is a cardiomyopathy. On the other hand, patients with severe anatomic AS may benefit from valve replacement despite the increased operative risk associated with a low-flow, low-gradient hemodynamic state. The recent American College of Cardiology/American Heart Association (ACC/AHA) guidelines for managing valvular heart disease recommends hemodynamic evaluation of low-flow, low-gradient AS using dobutamine echocardiography to distinguish patients with fixed anatomic AS from those with flow-dependent (“ relative”) AS in patients with LV …

Failed bioprosthetic valve approaches: Transcatheter aortic valve replacement approach

2019 AATS/ACC/ASE/SCAI/STS expert consensus systems of care document: A proposal to optimize care for patients with valvular heart disease: A joint report of the American Association for Thoracic Surgery, American College of Cardiology, American Society of Echocardiography, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons

Have We Entered the Era of “Code TAVR” and “Door-to-TAVR” Time?

Transcatheter Aortic Valve-in-Valve-in-Valve Implantation for a Failed Xenograft

Background— The prognostic impact of ECG left ventricular strain and left ventricular hypertrophy (LVH) in asymptomatic aortic stenosis is not well described. Methods and Results— Data were obtained in asymptomatic patients randomized to simvastatin/ezetimibe combination versus placebo in the Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) study. Primary end point was the first of myocardial infarction, nonhemorrhagic stroke, heart failure, aortic valve replacement, or cardiovascular death. The predictive value of ECG left ventricular strain (defined as T-wave inversion in leads V 4 through V 6 ) and LVH, assessed by Sokolow-Lyon voltage criteria (R V5–6 +S V1 ≥35 mV) and Cornell voltage-duration criteria {[RaVL+S V3 +(6 mV in women)]×QRS duration ≥2440 mV · ms}, was evaluated by adjustment for other prognostic covariates. A total of 1533 patients were followed for 4.3±0.8 years (6592 patient-years of follow-up), and 627 cardiovascular events occurred. ECG strain was present in 340 patients (23.6%), with LVH by Sokolow-Lyon voltage in 260 (17.1%) and by Cornell voltage-duration product in 220 (14.6%). In multivariable analyses, ECG left ventricular strain was associated with 3.1-fold higher risk of in-study myocardial infarction (95% confidence interval, 1.4–6.8; P =0.004). Similarly, ECG LVH by both criteria predicted, compared with no ECG LVH, 5.8-fold higher risk of heart failure (95% confidence interval, 2.0–16.8), 2.0-fold higher risk of aortic valve replacement (95% confidence interval, 1.3–3.1; both P =0.001), and 2.5-fold higher risk of a combined end point of myocardial infarction, heart failure, or cardiovascular death (95% confidence interval, 1.3–4.9; P =0.008). Conclusions— ECG left ventricular strain and LVH were independently predictive of poor prognosis in patients with asymptomatic aortic stenosis. Clinical Trial Registration— http://www.clinicaltrials.gov . Unique identifier: NCT00092677.

Clinical Summaries

Background: Long-standing aortic stenosis (AS) leads to elevated left ventricular (LV) pressure and as a consequence develops LV hypertrophy and increased myocardial fibrosis. The LV ejection fraction (LVEF) remains often preserved until the late stages of disease, but subtle LV dysfunction can be present in patients of severe AS. Transcatheter aortic valve replacement (TAVR) has become the primary method of aortic valve replacement for intermediate and high surgical risk patients with AS. In this study, we aimed to see if TAVR in patients with severe AS can result in the improvement of systolic functions. Subjects and Methods: We retrospectively studied the data of 52 consecutive symptomatic patients with severe symptomatic AS who underwent TAVR at our center. Echocardiography was performed at baseline and 6 months after the procedure to evaluate change in LVEF. Results: Fifty-two patients were retrospectively evaluated. The mean LVEF before TAVR was 49.52 ± 13.44. The mean LVEF after TAVR was 52.02 ± 10.95. That means there was a significant increase in LVEF after TAVR as compared to LVEF before TAVR (P = 0.008 using Wilcoxon signed-rank test). Conclusion: In this article, we conclude that, in AS patients, the removal of afterload by TAVR significantly improves cardiac functions as assessed by LVEF.

In this study we aimed to test the hypothesis that left ventricular (LV) afterload reduction in severe aortic valve stenosis (AS) by transcatheter aortic valve implantation (TAVI) acutely improves coronary haemodynamics. This was a prospective, pathophysiologic study in 40 patients with severe AS undergoing TAVI. Endpoints were determined invasively immediately before and after TAVI without altering coronary stenotic lesions if present. Myocardial hyperaemia was induced by intravenous adenosine. The primary study endpoints were coronary flow reserve (thermodilution-derived CFR), and fractional flow reserve (FFR). The secondary study endpoint was coronary collateral flow index (CFI) as obtained during a one-minute coronary balloon occlusion. CFR was 1.9±0.9 before TAVI and 2.0±1.0 after TAVI (p=0.72). FFR was 0.90±0.08 before TAVI and 0.93±0.08 after TAVI (p=0.0021). The TAVI-induced increase in FFR was related to a significant decrease in hyperaemic mean aortic pressure from 71±16 mmHg before TAVI to 67±15 mmHg after TAVI (p=0.0099). Hyperaemic CFI increased from 0.127±0.083 before to 0.146±0.090 after TAVI (p=0.0508). CFR appears not to be acutely affected by LV afterload reduction among patients with severe AS in response to TAVI. However, it acutely improves FFR; this occurs via lowering of mean aortic pressure. Hyperaemic coronary collateral flow index tends to augment in response to TAVI.

Aortic valve replacement surgery is the only available treatment option able to improve survival in patients with symptomatic and severe aortic valve stenosis. Without surgical intervention, patients with symptomatic dyspnea and severe aortic valve stenosis have a median survival less than 2 years. In an ideal, patient-centered healthcare system, the decision whether to undergo risky yet potentially life-prolonging surgery should not only reflect judicious application of the evidence of safety and efficacy of the surgery, but it also should be consistent with the patient’s clinical and personal contexts, and their goals, values, and preferences for life and healthcare. Article see p 533 The report by Bach et al1 is the latest in their series of investigations to uncover why cardiac valve replacement surgery is underused among eligible candidates. In this report, they seek explanations among patient, clinician, and hospital-level characteristics and suggest the following hypothesis: clinicians, particularly cardiologists, are making apparently inconsistent judgments as to which patients should be referred to cardiac surgeons for consideration of aortic valve replacement. Among 191 patients with severe aortic valve stenosis who did not undergo cardiac surgery, a cardiologist evaluated 182 (95%), but referred only 57 (30%) to a cardiac surgeon. In this editorial, we will place this finding in the context of the evolving field of shared decision-making and suggest how this focus could improve the quality of care delivered to patients with valvular heart disease. Shared decision making is a 3-step process.2 The first step involves knowledge transfer. In its idealized form, shared decision making requires symmetrical and bidirectional exchange of information between patients and clinicians. This exchange aims to identify and distinguish the available options under consideration, including the option of no treatment. The other 2 steps require the patient and clinician to (1) actively engage in deliberating (ie, …