Special topics: heart failure-related cardiogenic shock, valvular heart disease and end-stage renal disease. Part 4 of the International Expert Opinion Series on Acute Heart Failure Management.

Worldwide, valvular heart disease (VHD) is a common cause of hospitalization for acute heart failure. In acute heart failure caused by VHD, symptoms result from rapid haemodynamic changes and subsequent decline in cardiac function, and if left untreated, leads to acute decompensation and cardiogenic shock. Current evidence remains scarce and recommendations regarding the management of acute heart failure caused by VHD are lacking in most recent international guidelines. Herein, we review the management of acute heart failure caused by VHD with a focus on transcatheter therapies and describe currently available evidence based on a systematic literature search on the following valve pathologies: (i) aortic stenosis, (ii) aortic regurgitation, (iii) mitral regurgitation, and (iv) mitral stenosis. Articles reporting outcomes following urgent or emergent valve intervention in the setting of cardiogenic shock or acute heart failure were considered. After screening a total of 2234 articles, 76 published between 1994 and 2023 were included in subsequent analysis. Based on available evidence, proposed treatment algorithms to guide optimal management of acute heart failure caused by VHD were created. As the number of patients presenting with acute heart failure caused by VHD continues to rise and outcomes following transcatheter valve interventions continue to improve, it is inevitable that minimally invasive options will play an increasingly important role in the acute setting, especially given these patients are at an increased operative risk. This review aims to present an organized approach to the complex management and interventional treatment of patients with acute heart failure caused by VHD.

Case presentation: A 28-year-old woman with known mitral stenosis (MS) who was not taking antibiotic prophylaxis presented with new onset of chest pain, atrial fibrillation, and “heart failure.” She was treated for “heart failure” and converted spontaneously to sinus rhythm. Echocardiographic/Doppler studies showed a mitral valve gradient (MVG) of 7, a mitral valve area (MVA) of 1.2 cm2, 2+ mitral regurgitation (MR), no tricuspid regurgitation, normal left ventricular (LV) size and function, no left atrium (LA) thrombus, and a mitral valve score (University of Southern California [USC] scoring system) of 1, with no calcium in the commissures. At cardiac catheterization, mean pulmonary artery (PA) wedge was 23 mm Hg, mean PA pressure was 25 mm Hg, MVG was 10 mm Hg, and MVA was 1.2 cm2. On exercise, mean PA wedge was 30 mm Hg, mean PA pressure was 55 mm Hg, and MVG was 18 mm Hg. On angiography, the LV end-diastolic volume was 80 mL/m2, ejection fraction was 0.48, and 2+ MR, with normal coronary arteries. After catheter balloon commissurotomy (CBC), the MVA was 2.0 cm2, mean PA wedge was 13 mm Hg, and mean PA pressure was 20 mm Hg, with no MR. Her discharge medications were penicillin V 250 mg twice daily and antibiotic prophylaxis for prevention of infective endocarditis. ### Current Evaluations and Management of MS In almost all patients, MS is the result of previous rheumatic carditis with valve involvement. #### Severity of MS The relationship of the MVG as a function of the rate of mitral valve flow per diastolic second for various MVAs is shown in Figure 1. The threshold of onset of pulmonary edema is ∼20 mm Hg. Assuming a normal mean LV diastolic pressure (LVDP) of 5 mm Hg, a mean MVG of 20 mm Hg would be necessary1 to maintain …

American Society of Echocardiography Recommendations for the Use of Echocardiography in Rheumatic Heart Disease

Yes Is No

Temporal trends in the outcomes of acute heart failure: between consolatory evidences and real progress.

A cute severe valvular regurgitation is a surgical emer- gency, but accurate and timely diagnosis can be difficult.Although cardiovascular collapse is a common presentation, examination findings to suggest acute regurgitation may be subtle, and the clinical presentation may be nonspecific.Consequently, the presentation of acute valvular regurgitation may be mistaken for other acute conditions, such as sepsis, pneumonia, or nonvalvular heart failure.Although acute regurgitation may affect any valve, acute regurgitation of the left-sided valves is more common and has greater clinical impact than acute regurgitation of right-sided valves.Data to guide appropriate management of patients with acute regurgitation are sparse; there are no randomized trials, and much of the literature describes either small series or the experiences of specific centers.Despite these limitations, the available data are sufficient to allow identification of general principles as well as development of applicable guidelines from both the American College of Cardiology/American Heart Association and European Society of Cardiology.2][3] The data and guidelines emphasize overarching clinical principles, including the need for a high clinical suspicion of acute regurgitation, timely use of echocardiography, and, in the majority of patients, rapid progression to surgery. CausesCauses of acute regurgitation overlap with causes of chronic regurgitation and vary depending on the valve affected (Table 1).Endocarditis may affect either the aortic or mitral valve, whereas other causes are unique to the specific valve involved.The majority of causes of acute regurgitation present as an acute or subacute event.However, acute regurgitation can occur in patients with chronic regurgitation, when regurgitant severity is exacerbated by factors such as coronary ischemia, chordal rupture, or leaflet perforation from endocarditis.Acute regurgitation of either the aortic or mitral valve may result from procedural complications of percutaneous valve procedures.In addition, acute prosthetic valve regurgitation is seen more frequently as more patients undergo valve surgery.Acute prosthetic valve regurgitation is usually due to a tear of a bioprosthetic leaflet 4 or thrombosis of a mechanical valve, although perivalvular regurgitation can occur, particularly in prosthetic valve endocarditis.Acute aortic regurgitation is most commonly due to endocarditis, but there are a variety of less common causes as well.Aortic dissection, whether due to Marfan syndrome, bicuspid aortic valve, or atherosclerotic disease, may present with aortic regurgitation.Blunt trauma may result in leaflet rupture. 5Another less common cause is rupture of a fenestration in the aortic leaflet. 6cute mitral regurgitation may result from either "organic" or "functional" causes.Organic causes are those that result in permanent structural disruption of the valve, such as leaflet perforation from endocarditis, chordal rupture in myxomatous valve disease, or papillary muscle rupture due to myocardial infarction.Functional mitral regurgitation results from abnormalities of the left ventricle, such as cardiomyopathies in which the papillary muscles are laterally displaced, or acute ischemia, in which an akinetic wall segment and papillary muscle impair mitral valve closure.The distinction between organic and functional causes is an important one because treatment of organic causes requires surgical repair, whereas functional causes may improve with treatment of the underlying myocardial ischemia, infarction, or cardiomyopathy.Functional mitral regurgitation is more often chronic than acute.However, processes that result in rapid decline of ventricular function may cause acute functional mitral regurgitation as part of the presentation of acute heart failure.8][9] Emphasizing the variability in pathological process, a study demonstrated that mitral regurgitation in Takotsubo cardiomyopathy can result from outflow tract obstruction and systolic anterior mitral leaflet motion due to apical ballooning with preserved basal ventricular function. 9Rheumatic carditis can cause acute mitral regurgitation through a combination of leaflet inflammation and myocardial dysfunction, with some data suggesting that the degree of valve dysfunction drives outcomes. 10Although uncommon in industrialized nations, acute rheumatic carditis remains a significant issue in developing countries.

Assessment of the MitraClip Procedure: Reassessing the Goals

To the Editor, I am writing to express my appreciation for the recent publication by Umit Yuksek, "Red Cell Distribution Width Is an Independent Predictor of 1-Year Mortality in a Turkish Patient Population with Acute Decompensated Heart Failure" [1]. This study contributes significantly to our understanding of prognostic factors in acute heart failure, highlighting the importance of red cell distribution width (RDW) as an independent predictor of 1-year mortality in patients with acute decompensated heart failure. The methodology used in the study, which involved a cohort of 101 patients, provides an analysis of the predictive value of RDW as well as traditional clinical predictors. The finding that a 1% increase in RDW is associated with a 44% increase in 1-year mortality is particularly striking and emerging as a simple but powerful prognostic marker in clinical practice. In addition to the limitations mentioned by the author, there are a few other factors that could potentially impact the results. First, studies on the effect of demographic characteristics on the value of RDW show that RDW is associated with various clinical conditions and demographic factors [2]. It has been reported that RDW can be affected by a number of factors, such as age, gender, inflammation, coronary artery disease, heart failure, hyperlipidemia, diabetes mellitus, pneumonia, and chronic obstructive pulmonary disease. Patients with acute decompensated heart failure may also be frequently intertwined with these diseases during their initial admission. The fact that some of these important demographic characteristics were not clearly explained in the patient population of the study may be important in terms of influencing the results of the study. The criteria for inclusion or exclusion in the study are also not comprehensive and clear. We think that these should be specified in more detail. In addition, the non-invasive diagnosis of heart failure with preserved ejection fraction (HFpEF) is difficult and controversial. For this reason, it is recommended to use scoring systems like H2FPEF and HFA-PEFF for the diagnosis of HFpEF [3,4]. We believe that if any echocardiography or laboratory parameters other than the EF were evaluated while considering this patient group, it would be good to mention the methodology section. However, mentioning this issue in the limitations section may be useful if it is not mentioned. Second, when we look at the comparison of the clinical and laboratory characteristics of the subgroups with normal, high, and very high RDW values, it is noteworthy that factors such as Killip classification, mitral insufficiency, atrial fibrillation, cardiogenic shock, inotropic drug requirement, which may have significant effects on mortality in acute HEART FAILURE, do not have a significant relationship with high RDW. It also appears that even if it is not statistically significant, the EF value is positively correlated with RDW. As a result, despite this important success of RDW in showing a 1-year mortality estimate, it also has a weak relationship with many other mortality predictor parameters in acute heart failure, suggesting that unforeseen clinical conditions or parameters may potentially affect RDW in this study group. Statistically significant findings may not always be clinically or biologically significant. RDW may indicate that it is a clinically important variable, but this effect may be small and not make a significant difference in practice. The reason for coming to this conclusion is that the important limitations mentioned above may affect the study results. In conclusion, we believe that further research is necessary to investigate the mechanisms underlying the association between RDW and mortality in acute heart failure patients and to examine the potential of RDW to guide therapeutic interventions. We commend the author of this study, which not only enriches our understanding but also opens avenues for future research in acute heart failure management, and we thank the journal for publishing it. Yours sincerely

Background: Timely initiation of temporary mechanical circulatory support (tMCS), escalation and de-escalation strategies are key components for treatment of cardiogenic shock (CS). However, little is known about tMCS strategies and outcomes based on etiology of CS and chronicity of heart failure. We evaluated differences of tMCS strategies and outcome in patients supported with Impella in acute myocardial infarction related CS (AMI-CS), de novo heart failure related CS (de novo HF-CS), and acute on chronic heart failure related CS (acute on chronic HF-CS). Methods and Results: The Japan Registry for Percutaneous Ventricular Assist Device (J-PVAD) is multicenter, observational registry enrolling all consecutive patients treated with Impella in Japan. We conducted a retrospective analysis of patients with Impella in J-PVAD between February 2020 and December 2022. Among 3678 CS patients supported with Impella. 2418 (65.7%) patients were presented with AMI-CS, 758 (20.6%) patients with de novo HF-CS, and 502 (13.7%) patients with acute on chronic HF-CS. The median time from hospital entry to initiation of Impella were 127 min, 339 min, and 1117 min in AMI-CS, de novo HF-CS, and acute on chronic HF-CS, respectively (P < 0.001 for each). 2233 (92.4%) patients with AMI-CS underwent percutaneous coronary intervention during index hospitalization with median door-balloon-time of 108 min. Patients treated with multiple mechanical circulatory supports were 51.4%, 64.2%, and 55.2% in AMI-CS, de novo HF-CS, and acute on chronic HF-CS, respectively. Using de novo CS-HF as a reference, the risk for in-hospital mortality for AMI-CS and acute on chronic HF-CS were: odds ratio (OR) 1.24 [95% confidence interval (CI) 1.04–1.50], P = 0.02 and OR 1.43 (95% CI 1.12–1.81), P = 0.004, respectively. Conclusions: In CS patients supported with Impella, time course and utilization of tMCS varied in AMI-CS, de novo HF-CS, and acute on chronic HF-CS. De novo HF-CS had significantly better mortality relative to AMI-CS and acute-on-chronic CS. Further research is required for tMCS strategies based on etiology of CS and chronicity of heart failure.

Cardiac Anesthesiologist and Global Capacity Building to Tackle Rheumatic Heart Disease

Background The prevalence of valvular heart disease is on the rise. Severe valvular diseases are generally associated with high mortality, and aortic stenosis (AS) is associated with halved survival after out-of-hospital cardiac arrest (OHCA). Despite the severity of the prognosis of valvular heart diseases, their association with the risk of OHCA is not well-elucidated. Purpose The study aimed to examine the association between valvular heart disease and OHCA. Method We conducted a study using data from the nationwide Danish Cardiac Arrest Registry. We included adult OHCA patients with presumed cardiac origin. We compared OHCA cases with and without valvular heart disease, stratified by valvular disease type (AS, aortic regurgitation (AR), mitral stenosis (MS), and mitral regurgitation (MR) or multiple valvular diseases (more than 1 concomitant type of valvular disease)). We calculated the hazard ratios of OHCA using time-varying Cox regression models fitted with a nested case-control design. For each case, we matched up to five controls based on age, sex, year of OHCA, and two comorbidities: ischemic heart disease and congestive heart failure. Results We included 43,967 OHCA cases and 219,772 controls matched from the general population. In the total case population, the median age was 72 years, 68% were male, 26% had ischemic heart disease, 21% had congestive heart failure, and 57% had cardiovascular risk factors. We identified 1862 (4.23%) cases with AS, 336 (<1%) with AR, 31 with MS (<1%), 710 with MR (1.6%), and 605 with multiple valvular diseases (1.4%). Compared with cardiac arrest cases without valvular disease, cases with valvular disease were more likely to have ischemic heart disease (e.g., AS vs controls: 6.5% vs 1.7%, p<0.001) and congestive heart failure (e.g., MR vs controls: 3.5% vs 1%, p<0,001; AS vs controls: 8.2% vs 2.8%, p<0.001). AS, MS (HR: 1.67 [95%CI: 1.12; 2.51]), MR (HR: 1.38 [95%CI: 1.27; 1.50]) and multiple valvular diseases (HR: 1.36 [95%CI: 1.24; 1.49]) were significantly associated with higher hazard of OHCA (Figure 1); the strongest association was seen for AS (HR: 1.66 [95% CI: 1.58; 1.76]) (Figure 1). AR was not significantly associated with OHCA (HR: 1.05 [95%CI: 0.94; 1.19]). Conclusion In this Danish nationwide cardiac arrest cohort, aortic stenosis, aortic regurgitation, and mitral regurgitation were associated with increased rates of OHCA. The association was strongest in aortic stenosis patients. Focus on risk factors of OHCA in patients with valvular heart disease is warranted.Figure 1

Background: Breast cancer (BC) is the most common cause of cancer-related mortality among women. Despite advancements in treatment and longer survival, BC patients are at a higher risk of heart failure (HF) with an increased relative risk of 20% as compared to the general population. This has been attributed to cardiotoxicity from BC treatment and shared pathophysiological mechanisms. However, there is a need for more data on the outcomes of BC patients admitted with acute heart failure (AHF). Aim: To evaluate clinical outcomes, including in-hospital mortality, cardiogenic shock, respiratory failure, and length of stay (LOS), across different subtypes of AHF in BC patients. Methods: We analyzed the National Inpatient Sample database (2019-2022) to identify BC patients admitted with a primary diagnosis of AHF. AHF subtypes were classified into acute systolic heart failure (ASHF), acute diastolic heart failure (ADHF), combined ASHF/ADHF, and acute right heart failure (ARHF) based on ICD codes. Demographic information and clinical outcomes were collected and compared across AHF subtypes. Results: We identified 50,623 hospitalizations for AHF in patients with BC. The majority had ADHF only (55.6%), followed by ASHF (27.8%), combined ASHF/ADHF (16.1%), and ARHF (0.6%). The mean age across all groups was 77.8 years (SD ±10.2). In terms of racial distribution, most patients were White (73.6%), followed by Black (15.3%) and Hispanic (5.1%). The overall in-hospital mortality rate was 4.4%, with ARHF had the highest mortality at 12.2%, followed by ASHF (4.9%), combined ASHF/ADHF (4.5%), and ADHF (4.1%). Cardiogenic shock occurred in 2.6% of all AHF cases, most frequently in ARHF (8.2%) and ASHF (5.0%), and least in ADHF (1.0%). Respiratory failure was seen in 46.2% of all AHF patients—highest in ARHF (59.9%) and ADHF (50.3%). Mean LOS for AHF admissions was 6.11 days, ranging from 6.0 days in ASHF to 6.59 days in ARHF. Conclusion: Patients with ARHF had the highest rates of mortality, cardiogenic shock, respiratory failure, and the longest hospital stays, likely indicating a more severe clinical course. ADHF was the most common subtype but was associated with the lowest mortality and complication rates. These findings highlight the importance of recognizing AHF subtype in this population, as it may have significant implications for prognosis, management strategies, and healthcare resource allocation.

Developmental efforts to achieve percutaneous catheter-based therapies for cardiac valve repair and replacement have advanced rapidly over the past several years. A variety of methods to treat mitral regurgitation (MR) and to replace aortic and pulmonic valves have already been successfully employed in patients. These innovative clinical transcatheter valve therapies were anticipated more than a decade ago by creative experimentalists who helped develop predicate techniques in animal models. For example, in 1992, a catheter-delivered ball-in-cage prosthetic aortic valve was implanted in a canine model by Pavcnik1 and a stent-mounted bioprosthetic valve was placed by Andersen, who used a retrograde transarterial approach in a swine model.2 Clearly, the catheter-based technologies used in clinical studies today in patients with aortic stenosis were derived from the fusion of known successful aortic valve replacement (AVR) surgical devices and adaptive interventional modalities, first studied in experimental animal models. Similarly, approaches for transcatheter treatment of MR have also borrowed heavily from preexisting and accepted surgical techniques, such as the edge-to-edge leaflet coaptation technique and reduction ring mitral annuloplasty.3 Importantly, recognition that the coronary sinus parallels the mitral annulus has spurred unique catheter-based transvenous approaches to treat MR by indirectly reducing mitral annular dimensions.4 Because many of the new percutaneous approaches to valve therapy have been developed by surgeons, a collaboration has emerged between thoughtful surgeons and interventionalists, combining skill sets and experiences to accelerate the developmental pathways of less-invasive transcatheter valve therapies. Growing recognition exists that percutaneous alternatives to surgical therapies are required in some patient subgroups with valvular heart disease. Among patients with either mitral and/or aortic valve disease, an expanding population of elderly patients with significant comorbidities may benefit from traditional surgical methods, but these methods are associated with unacceptable perioperative mortality or prolonged postoperative recoveries. In the EuroHeart Survey …

Reprint of: Continuous renal replacement therapy and mild hypothermia for acute left heart failure after cardiovascular surgery

Outcomes With Femoral IABP in Heart Failure and Acute Myocardial Infarction-Related Cardiogenic Shock.