Outflow graft obstruction in patients with the HM 3 LVAD: A percutaneous approach.

BACKGROUND: The use of the HeartMate 3 (HM3) left ventricular assist device (LVAD) is expanding. Despite being associated with lower rates of adverse events and increased survival, outflow graft obstruction (OGO) has been reported in patients with HM3. The incidence and best management of this serious complication remain unclear. METHODS: We describe six cases of HM3 OGO occurring in five patients in our institutional HM3 cohort. Four cases underwent computed tomography angiography and in two percutaneous angiography was directly performed to confirm the diagnosis. In four cases, percutaneous repair of the OG was performed using common interventional cardiology (IC) techniques. RESULTS: Our institutional incidence of OGO was 7% (event rate of 0.05 per patient year); much higher than the previously reported incidence of 1.6%. All cases occurred in the bend relief covered segment. Only two patients had apparent OG twisting, and in two, OGO occurred despite placement of an anti-twist clip at the time of implant. External compression seems to play a role in most cases. Balloon "graftoplasty" and stent deployment via the femoral artery alleviated the obstruction and normalized LVAD flow in all patients who underwent percutaneous repair. The use of self-expanding stents allowed for downsizing of the procedural access site to 10 Fr. No serious procedure-related complications occurred. CONCLUSION: OGO is common in HM3 patients, external compression due to biomaterial accumulated surrounding the OG is a common etiology. Percutaneous repair using standard IC techniques is safe and feasible in cases of compression with or without partial twisting.

Diastolic function as an early marker for systolic dysfunction and all-cause mortality among cancer patients.

BACKGROUND: Increased survival among active cancer patients exposes a wide range of side effects, including cardiotoxicity, manifested by systolic dysfunction and associated with morbidity and mortality. Early diagnosis of subclinical function changes and cardiac damage is essential in the management of these patients. Diastolic dysfunction is considered common among cancer patients; however, its effect on systolic dysfunction or mortality is still unknown. METHODS: Data were collected as part of the Israel Cardio-Oncology Registry, enrolling and prospectively following all patients evaluated in the cardio-oncology clinic in the Tel Aviv Sourasky Medical Center. All patients underwent echocardiographic examinations including evaluation of diastolic parameters and global longitudinal strain (GLS). Systolic dysfunction was defined as either an absolute reduction >10% in left ventricular ejection fraction to a value below 53% or GLS relative reduction >10% between the 1st and 3rd echocardiography examinations. RESULTS: Overall, 190 active cancer patients were included, with a mean age of 58 ± 15 years and a female predominance (78%). During a median follow-up of 243 days (interquartile ranges [IQR]: 164-401 days), 62 (33%) patients developed systolic dysfunction. Over a median follow-up of 789 days (IQR: 521-968 days), 29 (15%) patients died. There were no significant differences in baseline cardiac risk factors between the groups. Using multivariate analysis, E/e' lateral and e' lateral emerged as significantly associated with systolic dysfunction development and all-cause mortality (P = .015). CONCLUSION: Among active cancer patients, evaluation of diastolic function may provide an early marker for the development of systolic dysfunction, as well as all-cause mortality.

C-Reactive Protein Velocity and the Risk of New Onset Atrial Fibrillation among ST Elevation Myocardial Infarction Patients.

BACKGROUND: Elevated C-reactive protein (CRP) was shown to be associated with an increased risk for new-onset atrial fibrillation (AF) in ST elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PCI); however, the optimal time frame to measure CRP for risk stratification is not known. OBJECTIVES: To evaluate the relation between the change in CRP over time (CRP velocity [CRPv]) and new-onset AF among STEMI patients treated with primary PCI. METHODS: We included 801 STEMI patients who underwent PCI between 2007 and 2017 and had their CRP measured with a wide range assay (wr-CRP) at least twice during the 24 hours after admission. CRPv was defined as the change in wr-CRP concentration (mg/l) divided by the change in time (in hours) between the two measurements. Patient medical records were reviewed for occurrence of new-onset AF. RESULTS: New onset AF occurred in 45 patients (6%). Patients with new onset AF had significantly higher median CRPv (1.27 vs. 0.43 mg/l/h, P = 0.002). New-onset AF during hospitalization occurred in 3.4%, 4.5 %, and 9.1% of patients in the first, second and third CRPv tertiles, respectively (P for trend = 0.006). In a multivariable logistic regression, adjusting for clinical variables the odds ratios for new onset AF was 1.93 (95% confidence interval 1.0-3.59, P = 0.04) for patients in the third CRPv tertile. CONCLUSIONS: CRPv might be an independent and rapidly measurable biomarker for new-onset AF following primary PCI in STEMI patients.

Cancer Therapeutics-Related Cardiac Dysfunction among Patients with Active Breast Cancer: A Cardio-Oncology Registry.

BACKGROUND: Progress in the treatment of breast cancer has led to substantial improvement in survival, but at the cost of increased side effects, with cardiotoxicity being the most significant one. The commonly used definition is cancer therapeutics-related cardiac dysfunction (CTRCD), defined as a left ventricular ejection fraction reduction of > 10%, to a value below 53%. Recent studies have implied that the incidence of CTRCD among patients with breast cancer is decreasing due to lower doses of anthracyclines and low association to trastuzumab and pertuzumab treatment. OBJECTIVES: To evaluate the prevalence of CTRCD among patients with active breast cancer and to identify significant associates for its development. METHODS: Data were collected as part of the Israel Cardio-Oncology Registry, which enrolls all patients who are evaluated at the cardio-oncology clinic at our institution. Patients were divided to two groups: CTRCD and no-CTRCD. RESULTS: Among 103 consecutive patients, five (5%) developed CTRCD. There were no significant differences in the baseline cardiac risk factors between the groups. Significant correlations of CTRCD included treatment with trastuzumab (P = 0.001) or pertuzumab (P < 0.001), lower baseline global longitudinal strain (GLS) (P = 0.016), increased left ventricular end systolic diameter (P < 0.001), and lower e' septal (P < 0.001). CONCLUSIONS: CTRCD is an important concern among patients with active breast cancer, regardless of baseline risk factors, and is associated with trastuzumab and pertuzumab treatment. Early GLS evaluation may contribute to risk stratification and allow deployment of cardioprotective treatment.

Association of pre-admission statin therapy and the inflammatory response in ST elevation myocardial infarction patients.

PURPOSE: To demonstrate the possible association of statin therapy with C reactive protein (CRP) serial measurements in ST elevation myocardial infarction (STEMI) patients. MATERIALS AND METHODS: STEMI patients between 2008 and 2016 with available CRP data from admission were divided into two groups according to pre-admission statin therapy. A second CRP measurement was noted following primary coronary intervention (within 24 h from admission). The difference between the two measurements was designated ΔCRP. RESULTS: The cohort consisted of 1134 patients with a median age of 61 (IQR52-70), 81% males. Patients on statins prior to admission (336/1134, 26%) were more likely to have CRP levels within normal range (≤5 mg/l) compared to patients without prior treatment, both at admission (75 vs. 24%, p = 0.004) and at 24 h (70 vs. 48%, p = 0.029). The prevalence of patients with pre-admission statin therapy decreased as ΔCRP increased (p = 0.004; n = 301). The likelihood of ΔCRP to be above 5 mg/l in patients with pre-admission statin therapy was reduced after age and gender adjustments (OR 0.54, 95% CI 0.32-0.92, p = 0.023) and in multivariate (OR 0.57, 95% CI 0.33-0.99, p = 0.048) analysis. CONCLUSIONS: Pre-admission statin therapy is associated with a less robust inflammatory response in STEMI patients, highlighting statin's pathophysiological importance.

Metabolic syndrome is associated to high-sensitivity cardiac troponin T elevation.

INTRODUCTION: Metabolic syndrome (MetS) and high-sensitivity cardiac troponin T (hs-TnT) are associated with higher risk for cardiovascular diseases (CVD). Our aim was to assess the relation between hs-TnT elevation and MetS in a general population sample. MATERIALS AND METHODS: Individuals participating in an annual health survey program between 2010 and 2016 were included in the study. Blood samples including hs-TnT levels were collected. The study population was divided into three groups based on hs-TnT levels - undetectable (<5 ng/L), intermediate (5-14 ng/L) and elevated (>14 ng/L). RESULTS: A total of 5994 subjects were included in the study, the mean age was 48.5 and 4336 (72%) were males. Compared with subjects with undetectable hs-TnT the prevalence of MetS was higher in those with detectable and elevated levels - 392 (10%) vs. 270 (15%) and 51 (33%), respectively (p < 0.001). In a multivariate model adjusted for age, gender and multiple co-morbidities, the number of MetS components and presence of MetS were significantly associated with an increased risk for detectable hs-TnT levels (OR = 1.02 {for each component}; 95% CI [1.00-1.05], p = 0.04) and (OR = 1.13; 95% CI [1.07-1.2], p < 0.001) respectively. Only the waist, glucose and hypertension components of the MetS were significantly associated with elevated troponin. CONCLUSIONS: The MetS and its distinct components have a cumulative impact on hs-TnT levels in apparently healthy subjects.

Elevated high-sensitive troponin T in negative stress test individuals.

BACKGROUND: The exercise ECG stress test (EST) is still the first step of work-up in intermediate risk patients in many clinical scenarios. High-sensitive cardiac troponin T (hs-cTnT) elevation is related to future cardiovascular events in the general population and in patients with ischaemic heart disease. The relation between these 2 tests is not well described. MATERIALS AND METHODS: A total of 2780 participants from the Tel-Aviv Medical Center Inflammation Survey cohort (mean age 49 years, 79% men) were analysed. Multiple physiologic and metabolic parameters including hs-cTnT were collected. All participants completed an EST manually reviewed by a cardiologist. RESULTS: A positive EST was documented in 224 subjects (8%). The majority (91%) of participants with hs-cTnT levels of 5-14 ng/L had a negative EST as well as 89.3% of subjects with levels >14 ng/L. The proportion of subjects with a positive EST and detectable hs-cTnT levels (>5 ng/L) was not significantly greater compared to those with a negative EST (53.1% vs 46.2%, respectively, P = .09). CONCLUSION: Among subjects referred for EST as part of an annual health survey, we found no significant association between EST results to hs-cTnT detection.

CRP velocity and short-term mortality in ST segment elevation myocardial infarction.

CONTEXT: There is a known association between C-reactive protein (CRP) levels and adverse outcomes in patients presenting with ST-elevation myocardial infarction (STEMI). The optimal time frame to measure CRP for risk stratification is not known. OBJECTIVE: The aim of the current study was to evaluate the relation between the change in CRP velocity (CRPv) and 30-d mortality among STEMI patients. MATERIAL AND METHODS: We included consecutive patients with a diagnosis of STEMI who presented to Tel-Aviv Medical Center between 2008 and 2014 and had their CRP measured with a wide range assay (wr-CRP) at least twice during the 24 h after admission. CRPv was defined as the change in wr-CRP concentration (mg/l) divided by the change in time (in hours) between the two measurements. RESULTS: The study population comprised of 492 patients, mean age was 62 ± 14, 80% were male. CRPv was significantly higher among patients who died within 30 d of admission (1.42 mg/l versus 0.18 mg/l, p < 0.001). In a multivariate regression model adjusted to multiple confounders, CRPv was independently associated with 30-d mortality (OR 1.39, 95% CI: 1.20-1.62, p < 0.001). CONCLUSION: CRPv might be an independent and rapidly measurable biomarker for short-term mortality in patients presenting with STEMI.

Exercise-induced albuminuria is related to metabolic syndrome.

Microalbuminuria (MA) is a known marker for endothelial dysfunction and future cardiovascular events. Exercise-induced albuminuria (EiA) may precede the appearance of MA. Associations between EiA and metabolic syndrome (MS) have not been assessed so far. Our aim was to investigate this association in a large sample of apparently healthy individuals with no baseline albuminuria. This was a cross-sectional study of 2,027 adults with no overt cardiovascular diseases who took part in a health survey program and had no baseline MA. Diagnosis of MS was based on harmonized criteria. All patients underwent an exercise test (Bruce protocol), and urinary albumin was measured before and after the examination. Urinary albumin-to-creatinine ratio (ACR) values before and after exercise were 0.40 (0.21-0.89) and 1.06 (0.43-2.69) mg/g for median (interquartile range) respectively. A total of 394 (20%) subjects had EiA; ACR rose from normal rest values (0.79 mg/g) to 52.28 mg/g after exercise (P < 0.001); this effect was not shown for the rest of the study population. EiA was related to higher prevalence of MS (13.8% vs. 27.1%, P < 0.001), higher metabolic equivalents (P < 0.001), higher baseline blood pressure (P < 0.001), and higher levels of fasting plasma glucose, triglycerides, and body mass index (P < 0.001). Multivariate binary logistic regression model showed that subjects with MS were 98% more likely to have EiA (95% confidence interval: 1.13-3.46, P = 0.016). In conclusion, EiA in the absence of baseline MA is independently related to MS.

Body mass index and the risk of new-onset atrial fibrillation in middle-aged adults.

BACKGROUND: Increased body mass index (BMI) and obesity are associated with increased risk of new-onset atrial fibrillation (AF) among middle-aged adults. OBJECTIVES: The objective of the study is to investigate the association between BMI and the risk for new-onset AF among middle-aged adults. METHODS: We investigated 18,290 men and women who were annually screened in a tertiary medical center. Participants were divided at baseline into 3 groups: normal weight (BMI ≥18 and <25 kg/m(2), n = 7,692), overweight (BMI ≥25 and <30 kg/m(2), n = 8,032), and obese (BMI ≥30 kg/m(2), n = 2,566). The primary end point was new-onset AF during follow-up. RESULTS: Mean age of study population was 49 ± 11 years, and 73% were men. A total of 288 incident events (1.6%) occurred during 6 ± 4 years. Kaplan-Meier survival analysis showed that the cumulative probability of AF at 6 years was highest among obese participants, intermediate among overweight participants, and lowest among participants with normal weight (2.1%, 1.7%, and 0.8% respectively, P < .001). Multivariable Cox regression analysis showed that overweight and obesity were independently associated with increased AF risk (hazard ratio 1.54 [P = .004] and 2.41 [P < .001], respectively). Assessment of BMI change as a time-dependent covariate in the multivariable model showed that each 1 kg/m(2) reduction in BMI during follow-up was associated with a significant 7% reduction in the risk for the occurrence of a first AF event (hazard ratio 0.93, 95% CI 0.88-0.99, P = .019). Consistently, similar analysis showed that each 5-kg weight loss during follow-up was independently associated with a significant 12% reduced risk of new-onset AF (95% CI 0.81-0.98, P = .02). CONCLUSIONS: Our findings suggest that overweight and obesity are associated with increased AF risk, whereas weight reduction is independently associated with reduced risk of de novo AF.

The association between cardiorespiratory fitness and cardiovascular risk may be modulated by known cardiovascular risk factors.

BACKGROUND: We aimed to evaluate whether reduced cardiovascular fitness has a direct or indirect effect for the development of cardiovascular disease. METHODS: We investigated 15,595 men and women who were annually screened in a tertiary medical center. All subjects were free of ischemic heart disease and had completed maximal exercise stress test according to the Bruce protocol at their first visit. Fitness was categorized into age- and sex-specific quintiles (Q) according to Bruce protocol treadmill time with Q1 as lowest fitness. Subjects were categorized at baseline into 3 groups: low fitness (Q1), moderate fitness (Q2-Q4), and high fitness (Q5). The primary end point of the current analysis was the development of a first cardiovascular event during follow-up. RESULTS: Mean age of study patients was 48 ± 10 years, and 73% were men. A total of 679 events occurred during 92,092 person-years of follow-up. Kaplan-Meier survival analysis showed that the cumulative probability of cardiovascular events at 6 years was significantly higher among subjects with low fitness (P < .001). Low fitness was associated with known cardiovascular risk factors, including hypercholesterolemia (odds ratio [OR] 1.58, 95% CI 1.31-1.89), diabetes mellitus (OR 2.32, 95% CI 1.58-3.41), and obesity (OR 10.46, 95% CI 8.43-12.98). The effect of low fitness on cardiovascular events was no longer significant when including diabetes mellitus, hypercholesterolemia, and obesity as mediators (hazard ratio 0.99, 95% CI 0.82-1.19). CONCLUSIONS: The association between cardiovascular fitness and adverse cardiovascular outcomes may be modulated through traditional cardiovascular risk factors. These findings need to be further validated in prospective clinical trials.

Impaired fasting glucose and left ventricular diastolic dysfunction in middle-age adults: a retrospective cross-sectional analysis of 2971 subjects.

BACKGROUND: Left ventricular (LV) diastolic dysfunction (LVDD) is a well-established and early echocardiographic characteristic of diabetic cardiomyopathy. However, there are limited data on the association between impaired fasting glucose (IFG) and LVDD. OBJECTIVE: To determine whether IFG is associated with LVDD among middle age adults. METHODS: Amongst 3781 subjects screened in an annual health survey program and referred for an echocardiogram, 2971 individuals without LV systolic dysfunction or valvular heart disease were selected. Mean age of study population was 59 ± 12 years and 75% were men. The subjects were categorized into three groups: euglycemia (N = 2025), IFG (N = 534) and diabetes mellitus (DM; N = 412). Doppler echocardiography readers were blinded to glycemic state. Subjects with impaired LV relaxation, pseudo-normal or restrictive filling patterns were defined as having LVDD. RESULTS: LVDD was diagnosed in 574 (19 %) of subjects and it was more prevalent among patients with IFG and DM than in euglycemic individuals (27, 30 and 15%, respectively; p < 0.001). Patients with IFG and DM had lower ratios of early (E) to late (A) trans-mitral flow (0.9 ± 0.3 and 0.9 ± 0.3 vs. 1.1 ± 0.4, respectively, p < 0.001). LV hypertrophy (LVH) was also more prevalent among patients with IFG and DM (11 and 18%, respectively, vs. 9%; p < 0.001). Multivariate binary logistic regression model adjusted to age, gender, obesity, LVH, renal function, total, high and low density lipoprotein cholesterol, triglycerides, ischemic heart disease, hypertension and LV ejection fraction showed that patients with IFG were 43% more likely to have LVDD compared with euglycemic subjects (95% confidence interval 1.12-1.83, p = 0.004). CONCLUSIONS: IFG is independently associated with a significant increase in the likelihood for the presence of LVDD in middle aged adults.

Anemia in ST-Elevation Myocardial Infarction Patients with Markers of Inadequate Bone Marrow Response.

BACKGROUND: Anemia confers an adverse prognosis in patients with ST-elevation myocardial infarction (STEMI). Several mechanisms have been implicated in the etiology of anemia in this setting, including inflammation, blood loss, and the presence of comorbidities such as renal failure. OBJECTIVES: To evaluate the adequacy of bone marrow response as potentially reflected by elevation in blood and reticulocyte counts. METHODS: Consecutive men with STEMI who underwent primary percutaneous intervention within 6 hours of symptom onset and who presented to our catheterization laboratory during a 36 month period were included in the study. The cohort was divided into quartiles according to hemoglobin concentration, and differences in clinical and laboratory characteristics between the groups were evaluated. RESULTS: A total of 258 men with STEMI were recruited, 22% of whom suffered from anemia according to the World Health Organization classification (hemoglobin < 13 g/dl). Men in the lowest quartile of hemoglobin concentration presented with significantly lower white blood cell and platelet counts (9.6 ± 2.9 vs. 12.6 ± 3.6 x 103/µl, P < 0.001) and (231 ± 79 vs. 263 ± 8 x 103/µl, P < 0.01), respectively, despite higher inflammatory biomarkers (C-reactive protein and fibrinogen) compared with patients in the upper hemoglobin concentration quartile. Reticulocyte production index was not significantly higher in anemic patients, with a value of 1.8, 1.4, 1.5 and 1.6 in the ascending hemoglobin quartiles, respectively (P = 0.292). CONCLUSIONS: Anemic men with STEMI have relatively lower leukocyte and platelet counts as well as a reduced reticulocyte count despite higher inflammatory biomarkers. These findings might suggest inadequate bone marrow response.

Self-rated health is associated with elevated C-reactive protein even among apparently healthy individuals.

BACKGROUND: A single self-rated health (SRH) assessment is associated with clinical outcome and mortality, but the biological process linking SRH with immune status remains incompletely understood. OBJECTIVES: To examine the association between SRH and inflammation in apparently healthy individuals. METHODS: Our analysis included 13,773 apparently healthy individuals attending the Tel Aviv Sourasky Medical Center for periodic health examinations. Estimated marginal means of the inflammation-sensitive biomarkers [i.e., highly sensitive C-reactive protein (hs-CRP) and fibrinogen] for the different SRH groups were calculated and adjusted for multiple potential confounders including risk factors, health behavior, socioeconomic status, and coexistent depression. RESULTS: The group with the lowest SRH had a significantly higher atherothrombotic profile and significantly higher conentrations of all inflammation-sensitive biomarkers in both genders. Hs-CRP was found to differ significantly between SRH groups in both genders even after gradual adjustments for all potential confounders. Fibrinogen differs significantly according to SRH in males only, with low absolute value differences. CONCLUSIONS: A valid association exists for apparently healthy individuals of both genders between inflammation-sensitive biomarker levels and SRH categories, especially when comparing levels of hs-CRP. Our findings underscore the importance of assessing SRH and treating it like other markers of poor health.

[Anemia in cardiovascular diseases: a prognostic marker or part of the disease?].

Many patients with cardiovascular diseases are anemic to some extent. Anemia is a well-known prognostic marker for negative outcome in a variety of atherosclerotic and hearts diseases. The detrimental outcome of anemic patients with cardiovascular diseases may be a consequence of the anemia, for instance as a pro-ischemic condition. However, anemia may indicate a pro-thrombotic and pro-inflammatory condition which contributes to the progression of cardiovascular diseases in general and atherosclerosis in particular. In this review we investigate the association between anemia and cardiovascular diseases, its mechanisms and how to utilize it for better understanding, prediction and treatment.

Prediction of recurrent heart failure hospitalizations and mortality using the echocardiographic Killip score.

AIM: Examine the performance of a simple echocardiographic "Killip score" (eKillip) in predicting heart failure (HF) hospitalizations and mortality after index event of decompensated HF hospitalization. METHODS: HF patients hospitalized at our facility between 03/2019-03/2021 who underwent an echocardiography during their index admission were included in this retrospective analysis. The cohort was divided into 4 classes of eKillip according to: stroke volume index (SVI) < 35ml/m2 > and E/E' ratio < 15 > . An eKillip Class I was defined as SVI ≥ 35ml/m2 and E/E' ≤ 15 and was used as reference. RESULTS: Included 751 patients, median age 78.1 (IQR 69.3-86) years, 59% men, left ventricular ejection fraction 45 (IQR 30-60)%, brain natriuretic peptide levels 634 (IQR 331-1222)pg/ml. Compared with eKillip Class I, a graded increase in the combined endpoint of 30-day mortality and rehospitalizations rates was noted: (Class II: HR 1.77, CI 0.95-3.33, p = 0.07; Class III: HR 1.94, CI 1.05-3.6, p = 0.034; Class IV: HR 2.9, CI 1.64-5.13, p < 0.001 respectively), which overall persisted after correction for clinical (Class II: HR 1.682, CI 0.9-3.15, p = 0.105; Class III: HR 2.104, CI 1.13-3.9, p = 0.019; Class IV: HR 2.74, CI 1.54-4.85, p = 0.001 respectively) or echocardiographic parameters (Class II: HR 1.92, CI 1.02-3.63, p = 0.045; Class III: HR 1.54, CI 0.81-2.95, p = 0.189; Class IV: HR 2.04, CI 1.1-3.76, p = 0.023 respectively). Specifically, the eKillip Class IV group comprised one-third of the patient population and persistently showed increased risk of 30-day HF hospitalizations or mortality following multivariate analysis. CONCLUSION: A simple echocardiographic score can assist identifying high-risk decompensated HF patients for recurrent hospitalizations and mortality.

Successful conservative management of left ventricular assist device candidates.

AIMS: Clinical trials comparing LVADs vs. conservative therapy were performed before the availability of novel medications or used suboptimal medical therapy. This study aimed to report that long-term stabilization of patients entering a left ventricular assist device (LVAD) programme is possible with the use of aggressive conservative therapy. This is important because the excellent clinical stabilization provided by LVADs comes at the expense of significant complications. METHODS AND RESULTS: This study was a single-centre prospective evaluation of consecutive patients with advanced heart failure (HF) fulfilling criteria for LVAD implantation based on clinical and echocardiographic characteristics, cardiopulmonary exercise test, and right heart catheterization results. Their initial therapy included inotropes, thiamine, beta-blockers, digoxin, spironolactone, hydralazine, and nitrates followed by the introduction of novel HF therapies. Coronary revascularization and cardiac resynchronization therapy were performed when indicated, and all patients were closely followed at our outpatient clinic. During the study period, 28 patients were considered suitable for LVAD implantation (mean age 63 ± 10.8 years, 92% men, 78% ischaemic, median HF duration 4 years). Clinical stabilization was achieved and maintained in 21 patients (median follow-up 20 months, range 9-38 months). Compared with baseline evaluation, cardiac index increased from 2.05 (1.73-2.28) to 2.88 (2.63-3.55) L/min/m2 , left ventricular end-diastolic diameter decreased from 65.5 (62.4-66) to 58.3 (53.8-62.5) mm, and maximal oxygen consumption increased from 10.1 (9.2-11.3) to 16.1 (15.3-19) mL/kg/min. Three patients died and only four ultimately required LVAD implantation. CONCLUSIONS: Notwithstanding the small size of our cohort, our results suggest that LVAD implantation could be safely deferred in the majority of LVAD candidates.

Medical Therapy for Functional Mitral Regurgitation.

Functional mitral regurgitation (FMR) can be broadly categorized into 2 main groups: ventricular and atrial, which often coexist. The former is secondary to left ventricular remodeling usually in the setting of heart failure with reduced ejection fraction or less frequently due to ischemic papillary muscle remodeling. Atrial FMR develops due to atrial and annular dilatation related to atrial fibrillation/flutter or from increased atrial pressures in the setting of heart failure with preserved ejection fraction. Guideline-directed medical therapy is the first step and prevails as the mainstay in the treatment of FMR. In this review, we address the medical therapeutic options for FMR management and highlight a targeted approach for each FMR category. We further address important clinical and echocardiographic characteristics to aid in determining when medical therapy is expected to have a low yield and an appropriate window for effective interventional approaches exists.

Echocardiographic Killip Classification.

BACKGROUND: Although routine echocardiographic parameters such as ejection fraction are used to risk-stratify for death in patients referred for echocardiography, they have limited predictive value. The authors speculated that noninvasive hemodynamic echocardiographic data, assessing left ventricular filling pressure and output, stratified on the basis of the clinical Killip score, might have additive prognostic value on top of routine echocardiographic parameters. The authors created an echocardiographic correlate of this classification, using diastolic grade and stroke volume index (SVI) as indicators of pulmonary congestion and systemic perfusion, respectively, and evaluated the prognostic value of this correlate. METHODS: A retrospective study of consecutive patients (hospitalized or not) referred for echocardiography for a range of cardiac diagnoses in a tertiary medical center. A total of 556 patients in sinus rhythm who were evaluated by two sonographers, and reviewed by a single cardiologist, were included. Normal filling pressure and normal SVI (>35 mL/m2) defined echocardiographic Killip (eKillip) class 1. Patients with pseudonormal or restrictive diastolic patterns and normal SVI were ascribed to eKillip class 2 or 3, respectively. A pseudonormal or restrictive diastolic pattern and a subnormal SVI defined eKillip class 4. RESULTS: eKillip class 1 was present in 382 patients (68%); 115 (20%), 26 (5%), and 42 (7%) patients were in eKillip classes 2 to 4, respectively. Median follow-up time was 1,056 days (interquartile range, 729-1,390 days). A total of 105 deaths occurred. Univariate Cox regression analysis showed that eKillip class was associated with all-cause mortality; hazard ratios (HR) -2.73 (95% CI, 1.67-4.48), 3.19 (95% CI, 1.42-7.17), and 4.79 (95% CI, 2.58-8.89) for each eKillip class above 1 (P < .001). In a multivariate analysis adjusted for the Charlson comorbidity index, eKillip class remained independently associated with all-cause mortality (P = .04). CONCLUSIONS: eKillip class was associated with all-cause mortality among all patients undergoing echocardiography at a tertiary hospital.