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ImportanceTransthyretin amyloid cardiomyopathy (ATTR-CM) is a form of heart failure (HF) with preserved ejection fraction (HFpEF). Technetium Tc 99m pyrophosphate scintigraphy (PYP) enables ATTR-CM diagnosis. It is unclear which patients with HFpEF have sufficient risk of ATTR-CM to warrant PYP.ObjectiveTo derive and validate a simple ATTR-CM score to predict increased risk of ATTR-CM in patients with HFpEF.Design, Setting, and ParticipantsRetrospective cohort study of 666 patients with HF (ejection fraction ≥ 40%) and suspected ATTR-CM referred for PYP at Mayo Clinic, Rochester, Minnesota, from May 10, 2013, through August 31, 2020. These data were analyzed September 2020 through December 2020. A logistic regression model predictive of ATTR-CM was derived and converted to a point-based ATTR-CM risk score. The score was further validated in a community ATTR-CM epidemiology study of older patients with HFpEF with increased left ventricular wall thickness ([WT] ≥ 12 mm) and in an external (Northwestern University, Chicago, Illinois) HFpEF cohort referred for PYP. Race was self-reported by the participants. In all cohorts, both case patients and control patients were definitively ascertained by PYP scanning and specialist evaluation.Main Outcomes and MeasuresPerformance of the derived ATTR-CM score in all cohorts (referral validation, community validation, and external validation) and prevalence of a high-risk ATTR-CM score in 4 multinational HFpEF clinical trials.ResultsParticipant cohorts included were referral derivation (n = 416; 13 participants [3%] were Black and 380 participants [94%] were White; ATTR-CM prevalence = 45%), referral validation (n = 250; 12 participants [5%]were Black and 228 participants [93%] were White; ATTR-CM prevalence = 48% ), community validation (n = 286; 5 participants [2%] were Black and 275 participants [96%] were White; ATTR-CM prevalence = 6% ), and external validation (n = 66; 23 participants [37%] were Black and 36 participants [58%] were White; ATTR-CM prevalence = 39%). Score variables included age, male sex, hypertension diagnosis, relative WT more than 0.57, posterior WT of 12 mm or more, and ejection fraction less than 60% (score range −1 to 10). Discrimination (area under the receiver operating characteristic curve [AUC] 0.89; 95% CI, 0.86-0.92; P 2 = 4.6; P = .46) were strong. Discrimination (AUC ≥ 0.84; P 2 = 2.8; P = .84; Hosmer-Lemeshow χ2 = 4.4; P = .35; Hosmer-Lemeshow χ2 = 2.5; P = .78 in referral, community, and external validation cohorts, respectively) were maintained in all validation cohorts. Precision-recall curves and predictive value vs prevalence plots indicated clinically useful classification performance for a score of 6 or more (positive predictive value ≥25%) in clinically relevant ATTR-CM prevalence (≥10% of patients with HFpEF) scenarios. In the HFpEF clinical trials, 11% to 35% of male and 0% to 6% of female patients had a high-risk (≥6) ATTR-CM score.Conclusions and RelevanceA simple 6 variable clinical score may be used to guide use of PYP and increase recognition of ATTR-CM among patients with HFpEF in the community. Further validation in larger and more diverse populations is needed.

Importance: Diagnosis of heart failure with preserved ejection fraction (HFpEF) among dyspneic patients without overt congestion is challenging. Multiple diagnostic approaches have been proposed but are not well validated against the independent gold standard for HFpEF diagnosis of an elevated pulmonary capillary wedge pressure (PCWP) during exercise. Objective: To evaluate H 2FPEF and HFA-PEFF scores and a PCWP/cardiac output (CO) slope of more than 2 mm Hg/L/min to diagnose HFpEF. Design, Setting, and Participants: This retrospective case-control study included patients with unexplained dyspnea from 6 centers in the US, the Netherlands, Denmark, and Australia from March 2016 to October 2020. Diagnosis of HFpEF (cases) was definitively ascertained by the presence of elevated PCWP during exertion; control individuals were those with normal rest and exercise hemodynamics. Main Outcomes and Measures: Logistic regression was used to evaluate the accuracy of HFA-PEFF and H 2FPEF scores to discriminate patients with HFpEF from controls. Results: Among 736 patients, 563 (76%) were diagnosed with HFpEF (mean [SD] age, 69 [11] years; 334 [59%] female) and 173 (24%) represented controls (mean [SD] age, 60 [15] years; 109 [63%] female). H 2FPEF and HFA-PEFF scores discriminated patients with HFpEF from controls, but the H 2FPEF score had greater area under the curve (0.845; 95% CI, 0.810-0.875) compared with the HFA-PEFF score (0.710; 95% CI, 0.659-0.756) (difference, -0.134; 95% CI, -0.177 to -0.094; P 2FPEF score. Use of the PCWP/CO slope to redefine HFpEF rather than exercise PCWP reclassified 20% (117 of 583) of patients, but patients reclassified from HFpEF to control by this metric had clinical, echocardiographic, and hemodynamic features typical of HFpEF, including elevated resting PCWP in 66% (46 of 70) of reclassified patients. Conclusions and Relevance: In this case-control study, despite requiring fewer data, the H 2FPEF score had superior diagnostic performance compared with the HFA-PEFF score and PCWP/CO slope in the evaluation of unexplained dyspnea and HFpEF in the outpatient setting..

Pericardial effusions can result in acute hemodynamic compromise and require rapid intervention. Understanding pericardial restraint is essential to determine the approach to newly identified pericardial effusions in the intensive care unit. As pericardial effusions stretch the pericardium, pericardial compliance reserve is eventually exhausted, with an exponential rise in compressive pericardial pressure. The severity of pericardial pressure increase depends on both the rapidity and volume of pericardial fluid accumulation. This increase in pericardial pressure is reflected in an increase in measured left and right sided ‘filling’ pressures, but paradoxically left ventricular end diastolic volume (the true left ventricular preload) is decreased. This uncoupling of filling pressures and preload is the hallmark of pericardial restraint. When this occurs acutely from a pericardial effusion, rapid recognition and pericardiocentesis can be lifesaving. In this review, we will discuss the hemodynamics and pathophysiology of acute pericardial effusions, provide a physiological guide to determine need for pericardiocentesis in acute care, and discuss important caveats to management.

Mitral transcatheter edge-to-edge repair (MTEER) is an established therapeutic approach for mitral regurgitation (MR). Functional mitral regurgitation originating from atrial myopathy (A-FMR) has been described.We sought to assess the clinical, echocardiographic and hemodynamic considerations in A-FMR patients undergoing MTEER.From 2014 to 2020, patients undergoing MTEER for degenerative MR (DMR), functional MR (FMR), and mixed MR were assessed. A-FMR was defined by the presence of MR moderate in severity; left ventricular (LV) ejection fraction (LVEF) ≥ 50%; and severe left atrial (LA) enlargement in the absence of LV dysfunction, leaflet pathology, or LV tethering. The diagnosis of A-FMR (vs. ventricular-FMR [V-FMR]) was confirmed by three independent echocardiographers. Baseline characteristics, procedural outcomes as well as clinical and echocardiographic follow-up are reported. Device success was defined as final MR grade ≤ moderate; MR reduction ≥1 grade; and final transmitral gradient5 mmHg.306 patients underwent MTEER, including DMR (62%), FMR (19%), and mixed MR (19%). FMR cases included 37 (63.8%) V-FMR and 21 (36.2%) A-FMR. Tricuspid regurgitation (≥ moderate) was higher in A-FMR (80.1%) compared to V-FMR (54%) and DMR (42%). Device success did not significantly differ between A-FMR and V-FMR (57% vs. 73%, p = 0.34) or DMR (57% vs. 64%, p = 1.0). The A-FMR cohort was less likely to achieve ≥3 grades of MR reduction compared to V-FMR (19% vs. 54%, p = 0.01) and DMR (19% vs. 49.7%, p = 0.01). Patients with V-FMR and DMR demonstrated significant reductions in mean left atrial pressure (LAP) and peak LA V-wave, though A-FMR did not (LAP -0.24 ± 4.9, p = 0.83; peak V-wave -1.76 ± 9.1, p = 0.39). In follow-up, echocardiographic and clinical outcomes were similar.In patients undergoing MTEER, A-FMR represents one-third of FMR cases. A-FMR demonstrates similar procedural success but blunted acute hemodynamic responses compared with DMR and V-FMR following MTEER. Dedicated studies specifically considering A-FMR are needed to discern the optimal therapeutic approaches.

Aims Pulmonary hypertension (PH) has been consistently associated with adverse outcomes in hospitalized patients. Limited epidemiologic data exist regarding PH in the cardiac intensive care unit (CICU) population. Here, we describe the prevalence, aetiology, and outcomes of PH in the CICU. Methods and results Cardiac intensive care unit patients admitted from 2007 to 2018 who had right ventricular systolic pressure (RVSP) measured via transthoracic echocardiography near CICU admission were included. PH was defined as RVSP >35 mmHg, and moderate-to-severe PH as RVSP ≥50 mmHg. Predictors of in-hospital mortality were determined using multivariable logistic regression. Among 5042 patients (mean age 69.4 ± 14.8 years; 41% females), PH was present in 3085 (61%). The majority (68%) of patients with PH had left heart failure, and 29% had lung disease. In-hospital mortality occurred in 8.3% and was more frequent in patients with PH [10.9% vs. 4.2%, adjusted odds ratio (OR) 1.40, 95% confidence interval (CI) 1.03–1.92, P = 0.03], particularly patients with moderate-to-severe PH (14.4% vs. 6.2%, adjusted OR 1.65, 95% CI 1.27–2.14, P Conclusions Pulmonary hypertension is very common in the CICU population and appears to be independently associated with a higher risk of death during hospitalization, although the strength of this association varies according to the underlying admission diagnosis. These data highlight the importance of PH in patients with cardiac critical illness.

Heart failure with preserved ejection fraction (HFpEF) is a common disorder with few effective treatments. There is currently no evidence-based method to identify preclinical HFpEF. The H2FPEF score is a validated instrument to identify patients with overt HFpEF. Here we show the H2FPEF score can identify individuals with preclinical HFpEF. Among individuals where heart failure was excluded (n=160), increasing H2FPEF score was shown to be associated with greater left atrial dilation, left ventricular hypertrophy, and more severe diastolic dysfunction. Patients with increasing H2FPEF score displayed higher pulmonary artery pressures, higher left heart filling pressures, lower cardiac index, and more severely impaired aerobic capacity during exercise. In summary, we show that among adults without heart failure, higher H2FPEF score is associated with subclinical abnormalities that resemble those observed in HFpEF. These findings broaden the external validity of the H2FPEF score and suggest that this instrument may help identify patients positioned to benefit from preventive interventions.

Aims Pulmonary hypertension (PH) and pulmonary vascular disease (PVD) are common and associated with adverse outcomes in left heart disease (LHD). This study sought to characterize the pathophysiology of PVD across the spectrum of PH in LHD. Methods and results Patients with PH-LHD [mean pulmonary artery (PA) pressure >20 mmHg and PA wedge pressure (PAWP) ≥15 mmHg] and controls free of PH or LHD underwent invasive haemodynamic exercise testing with simultaneous echocardiography, expired air and blood gas analysis, and lung ultrasound in a prospective study. Patients with PH-LHD were divided into isolated post-capillary PH (IpcPH) and PVD [combined post- and pre-capillary PH (CpcPH)] based upon pulmonary vascular resistance (PVR Conclusions Pulmonary vascular disease in LHD is associated with a distinct pathophysiologic signature marked by greater exercise-induced lung congestion, arterial hypoxaemia, RV–PA uncoupling, ventricular interdependence, and impairment in O2 delivery, impairing aerobic capacity. Further study is required to identify novel treatments targeting the pulmonary vasculature in PH-LHD.

Background A patent foramen ovale (PFO) is a persistent embryonic defect in the interatrial septum. Platypnoea-orthodeoxia syndrome is characterized by positional hypoxaemia that is most commonly due to right-to-left shunting through a PFO. Dynamic right-to-left shunting through a PFO can also exacerbate positional hypoxaemia without platypnea-orthodeoxia syndrome. Case summary A 78-year-old woman with hyperthyroidism and paroxysmal atrial fibrillation (AF) presented with positional hypoxaemia exacerbated by supine positioning. Diagnostic testing revealed intermittent right-to-left shunting through a PFO triggered by worsening atrial functional tricuspid regurgitation and elevated right atrial pressures. Diuresis, rate control, and thyroidectomy initially led to resolution of positional hypoxaemia, but recurrent AF episodes triggered right-to-left shunting with recurrent desaturation. Left atrial and cavo-tricuspid isthmus ablation led to restoration of normal sinus rhythm and resolution of positional hypoxaemia without PFO closure. Discussion The clinical presentation of intermittent intracardiac right-to-left shunting can mimic decompensated heart failure with pulmonary oedema. Persistent hypoxaemia out of proportion to the degree of pulmonary oedema and minimally responsive to supplemental O2 should raise suspicion for right-to-left shunt aetiology. Positional arterial blood gases can facilitate the diagnostic evaluation of refractory hypoxaemia in cases of suspected shunting. Diagnostic imaging for PFO detection includes both transthoracic and transesophageal echocardiography with Valsalva manoeuver and agitated saline injection. Closure of a PFO for management of arterial deoxygenation syndromes should not be performed before treating other causes of arterial deoxygenation and optimizing factors that may exacerbate shunting across the PFO.

Background A substantial proportion of patients with heart failure (HF) with preserved ejection fraction (HFpEF) present with normal natriuretic peptide (NP) levels. The pathophysiology and natural history for this phenotype remain unclear. Methods and results Consecutive subjects undergoing invasive cardiopulmonary exercise testing for unexplained dyspnoea at Mayo Clinic in 2006-18 were studied. Heart failure with preserved ejection fraction was defined as a pulmonary arterial wedge pressure (PAWP) >= 15 mmHg (rest) or >= 25 mmHg (exercise). Patients with HFpEF and normal NP [N-terminal of the pro-hormone B-type natriuretic peptide (NT-proBNP) < 125 ng/L] were compared with HFpEF with high NP (NT-proBNP >= 125 ng/L) and controls with normal haemodynamics. Patients with HFpEF and normal (n = 157) vs. high NP (n = 263) were younger, yet older than controls (n = 161), with an intermediate comorbidity profile. Normal NP HFpEF was associated with more left ventricular hypertrophy and worse diastolic function compared with controls, but better diastolic function, lower left atrial volumes, superior right ventricular function, and less mitral/tricuspid regurgitation compared with high NP HFpEF. Cardiac output (CO) reserve with exercise was preserved in normal NP HFpEF [101% predicted, interquartile range (IQR): 75-124%], but this was achieved only at the cost of higher left ventricular transmural pressure (LVTMP) (14 +/- 6 mmHg vs. 7 +/- 4 mmHg in controls, P < 0.001). In contrast, CO reserve was decreased in high NP HFpEF (85% predicted, IQR: 59-109%), with lower LVTMP (10 +/- 8 mmHg) compared with normal NP HFpEF (P < 0.001), despite similar PAWP. Patients with high NP HFpEF displayed the highest event rates, but normal NP HFpEF still had 2.7-fold higher risk for mortality or HF readmissions compared with controls (hazard ratio: 2.74, 95% confidence interval: 1.02-7.32) after adjusting for age, sex, and body mass index. Conclusion Patients with HFpEF and normal NP display mild diastolic dysfunction and preserved CO reserve during exercise, despite marked elevation in filling pressures. While clinical outcomes are not as poor compared with patients with high NP, patients with normal NP HFpEF exhibit increased risk of death or HF readmissions compared with patients without HF, emphasizing the importance of this phenotype. Key question What is the prognosis of patients with heart failure and preserved ejection fraction (HFpEF) who have normal natriuretic peptide (NP) levels? How does this group present in terms of cardiac structure and function, and haemodynamics at rest and during exercise? Key finding Patients with HFpEF and normal NP levels have increased mortality and heart failure readmissions compared with subjects with non-cardiac dyspnoea. Heart failure and preserved ejection fraction with elevated vs. normal NP levels is associated with worse right ventricular function, more secondary valve regurgitation, and impaired cardiac output reserve. Take-home message A considerable number of patients with HFpEF present with normal NP levels. Those patients exhibit increased morbidity and mortality in comparison with patients without heart failure, emphasizing the importance of this phenotype. F.H.V. is supported by a Fellowship of the Belgian American Educational Foundation (B.A.E.F.) and by the Special Research Fund (BOF) of Hasselt University (BOF19PD04). B.A.B. is supported by R01 HL128526 from the National Institutes of Health. The authors thank the staff of the Earl Wood Catheterization Laboratory and the patients who agreed to participate in research, allowing for this study to be completed.

ImportanceReduced heart rate during exercise is common and associated with impaired aerobic capacity in heart failure with preserved ejection fraction (HFpEF), but it remains unknown if restoring exertional heart rate through atrial pacing would be beneficial.ObjectiveTo determine if implanting and programming a pacemaker for rate-adaptive atrial pacing would improve exercise performance in patients with HFpEF and chronotropic incompetence.Design, Setting, and ParticipantsSingle-center, double-blind, randomized, crossover trial testing the effects of rate-adaptive atrial pacing in patients with symptomatic HFpEF and chronotropic incompetence at a tertiary referral center (Mayo Clinic) in Rochester, Minnesota. Patients were recruited between 2014 and 2022 with 16-week follow-up (last date of follow-up, May 9, 2022). Cardiac output during exercise was measured by the acetylene rebreathe technique.InterventionsA total of 32 patients were recruited; of these, 29 underwent pacemaker implantation and were randomized to atrial rate responsive pacing or no pacing first for 4 weeks, followed by a 4-week washout period and then crossover for an additional 4 weeks.Main Outcomes and MeasuresThe primary end point was oxygen consumption (V̇o2) at anaerobic threshold (V̇o2,AT); secondary end points were peak V̇o2, ventilatory efficiency (V̇e/V̇co2 slope), patient-reported health status by the Kansas City Cardiomyopathy Questionnaire Overall Summary Score (KCCQ-OSS), and N-terminal pro-brain natriuretic peptide (NT-proBNP) levels.ResultsOf the 29 patients randomized, the mean age was 66 years (SD, 9.7) and 13 (45%) were women. In the absence of pacing, peak V̇o2 and V̇o2 at anaerobic threshold (V̇o2,AT) were both correlated with peak exercise heart rate (r = 0.46-0.51, P P P o2,AT (pacing off, 10.4 [SD, 2.9] mL/kg/min; pacing on, 10.7 [SD, 2.6] mL/kg/min; absolute difference, 0.3 [95% CI, −0.5 to 1.0] mL/kg/min; P = .46), peak V̇o2, minute ventilation (V̇e)/carbon dioxide production (V̇co2) slope, KCCQ-OSS, or NT-proBNP level. Despite the increase in heart rate, atrial pacing had no significant effect on cardiac output with exercise, owing to a decrease in stroke volume (−24 mL [95% CI, −43 to −5 mL]; P = .02). Adverse events judged to be related to the pacemaker device were observed in 6 of 29 participants (21%).Conclusions and RelevanceIn patients with HFpEF and chronotropic incompetence, implantation of a pacemaker to enhance exercise heart rate did not result in an improvement in exercise capacity and was associated with increased adverse events.Trial RegistrationClinicalTrials.gov Identifier: NCT02145351

Research in the last decade has substantially advanced our understanding of the pathophysiology of heart failure with preserved ejection fraction (HFpEF). However, treatment options remain limited as clinical trials have largely failed to identify effective therapies. Part of this failure may be related to mechanistic heterogeneity. It is speculated that categorizing HFpEF patients based upon underlying pathophysiological phenotypes may represent the key next step in delivering the right therapies to the right patients. Echocardiography may provide valuable insight into both the pathophysiology and underlying phenotypes in HFpEF. Echocardiography also plays a key role in the evaluation of patients with unexplained dyspnea, where HFpEF is suspected but the diagnosis remains unknown. The combination of the E/e' ratio and right ventricular systolic pressure has recently been shown to add independent value to the diagnostic evaluation of patients suspected of having HFpEF. Finally, echocardiography enables identification of the different causes that mimic HFpEF but are treated differently, such as valvular heart disease, pericardial constriction, and high-output heart failure or infiltrative myopathies such as cardiac amyloid. This review summarizes the current understanding of the pathophysiology and phenotyping of HFpEF with particular attention to the role of echocardiography in this context.

Prashanth Rajagopalan,1 Georgi Abraham,2 Yuvaram NV Reddy,2 Ravivarman Lakshmanasami,1 ML Prakash,1 Yogesh NV Reddy2 1Department of General Medicine, Mahatma Gandhi Medical College and Research Institute, Puducherry, 2Department of Nephrology, Madras Medical Mission Hospital, Chennai, India Abstract: This population-based prospective study was undertaken in Mahatma Gandhi Medical College to estimate the renal function in young healthy Indian adults. A young healthy heterogeneous Indian cohort comprising 978 individuals, predominantly medical students, was assessed by a detailed questionnaire, and variables such as height, weight, body mass index (BMI), birth weight, and blood pressure were documented. Laboratory investigations included serum creatinine, serum cystatin C, blood sugar, urine protein, and imaging of the kidneys with ultrasound. The mean age of the cohort was 25±6years, comprising 672 males and 306 females. The estimated glomerular filtration rates (eGFRs) by the Cockcroft–Gault formula for BMI

Pulmonary vascular resistance fails to decrease appropriately during exercise in patients with heart failure with preserved ejection fraction (HFpEF). Interventions that enhance pulmonary vasodilation might be beneficial in this cohort but could also worsen left atrial hypertension, exacerbating lung congestion. Intravenous β-agonists reduce pulmonary vascular resistance but are not suitable for chronic use.We hypothesized that the inhaled β-adrenergic agonist albuterol would improve pulmonary vasodilation during exercise in patients with HFpEF, without increasing left heart filling pressures.We performed a randomized, double-blind, placebo-controlled trial testing the effects of inhaled albuterol on resting and exercise hemodynamics in subjects with HFpEF using high-fidelity micromanometer catheters and expired gas analysis. The primary end point was pulmonary vascular resistance during exercise. Subjects with HFpEF (n=30) underwent resting and exercise hemodynamic assessment and were then randomized 1:1 to inhaled, nebulized albuterol or placebo. Rest and exercise hemodynamic testing was then repeated. Albuterol improved the primary end point of exercise pulmonary vascular resistance as compared with placebo (-0.6±0.5 versus +0.1±0.7 WU; P=0.003). Albuterol enhanced cardiac output reserve and right ventricular pulmonary artery coupling, reduced right atrial and pulmonary artery pressures, improved pulmonary artery compliance, and enhanced left ventricular transmural distending pressure (all P0.01), with no increase in pulmonary capillary hydrostatic pressures.Albuterol improves pulmonary vascular reserve in patients with HFpEF without worsening left heart congestion. Further study is warranted to evaluate the chronic efficacy of β-agonists in HFpEF and other forms of pulmonary hypertension.URL: http://www.clinicaltrials.gov . Unique identifier: NCT02885636.

Catheter ablation is a well-established treatment for atrial fibrillation (AF). A subset of patients developed dyspnea secondary to loss of left atrial (LA) compliance after ablation, which is referred as the stiff LA syndrome.(1) Stiff left atrium syndrome has traditionally been associated with profound eccentric LA remodeling. We report the case of a patient with this clinical syndrome who developed giant V-waves during exercise but had a strikingly small LA.

Patients with heart failure (HF) and reduced ejection fraction (HFrEF) display exercise intolerance measured objectively as decreased peak oxygen uptake (VO2).1 In accordance with Fick’s principal and law of diffusion, reduced peak VO2 is the result of impaired convective and diffusive O2 transport.2,3 Endurance training improves peak VO2 in clinically stable HFrEF patients secondary to central and peripheral adaptations that result in increased cardiac output and O2 distribution and extraction in skeletal muscle.1 We report, using invasive hemodynamic and pulmonary gas exchange measures, exercise changes in VO2 and its determinants in an avid cyclist with severe cardiac limitation because of advanced HFrEF. A 55-year-old male patient who had been a lifelong marathon runner was diagnosed with idiopathic nonischemic dilated cardiomyopathy 5 years before evaluation. He had a history of atrial fibrillation and was on optimal doses of carvedilol, lisinopril, and spironolactone. His ejection fraction was 20% to 25%, but he had remained in New York Heart Association class I and was able to continue cycling and intense daily exercise. In the past year, he was hospitalized twice for acutely decompensated HF, with gradually worsening effort intolerance. Given the increasing need for hospitalization, he was referred for invasive exercise testing as part of a transplant evaluation workup. Laboratories revealed hemoglobin 13.3 g/dL, creatinine 1.5 mg/dL, sodium 132 mmol/L, troponin 0.06 ng/mL, and NT-proBNP (N-terminal pro-B-type natriuretic peptide) 14 080 pg/mL. Echocardiography showed ejection …

Mitral valve regurgitation (MR) is the most common valvular heart disease. Primary MR is a disease of the mitral valve apparatus, whereas secondary MR is a disease of the left ventricle. Diagnosing and managing MR is often challenging and requires a structured approach, integrating findings on history, physical examination, and imaging. Decisions regarding treatment depend on knowledge of the etiology, natural history, and outcome of interventions for these patients with mitral valve disease. The optimal timing of intervention requires a comprehensive 2-dimensional and Doppler echocardiogram in each patient to determine the cause of the mitral valve disease, the severity of the regurgitation, and the effect of the volume overload on the left ventricle, as well as determining if a durable valve repair can be performed. Advances in both surgical and catheter-based therapies have resulted in recommendations for lower thresholds for operation and extension of interventional treatments to the older, sicker population of patients with MR. The current review discusses the pathophysiological rationale for current diagnostic and management strategies in MR.

The aim of this retrospective study was to compare the prevalence of pulmonary hypertension in a cohort of patients with end-stage renal disease (ESRD) prior to and following renal transplantation and to identify the possible risk factors. Of the 425 renal transplantations performed between 2001 and 2007, Doppler echocardiographic findings were available in 124. The echocardiographic data, collected both pre- and post-transplant, included the pulmonary artery pressure (PAP), ejection fraction and left ventricular hypertrophy. The data analyzed included age, gender, hypertension, diabetes, smoking status, along with blood urea, creatinine, glomerular filtration rate, hemoglobin, hemodialysis duration, urine albumin, arterio-venous access and body mass index (BMI). Chi-square test was used for discrete variables and ANOVA was used for continuous variables. Of the patients studied, males comprised 72%; the mean age was 43.3 ± 13.02 years; 87% were hypertensive, 30% were diabetic and 4% were smokers. Statistical analysis revealed a significant reduction of the PAP, irrespective of its severity, following renal transplantation (P

Patients with advanced heart failure (HF) are predisposed to ventricular arrhythmias (VAs), particularly following implantation of a left ventricular assist device (LVAD). There is minimal evidence for appropriate management strategies.This study aimed to compare the burden of VA and response to ablation performed either before or following LVAD implantation.We created a retrospective cohort of patients who underwent both VA ablation and Heart Mate II (Thoratec, Pleasanton, CA, USA) LVAD implantation at Mayo Clinic (Rochester, MN, USA). Patients were stratified based on whether they underwent VA ablation before (pre-LVAD) or after LVAD (post-LVAD) implantation. Descriptive analyses assessed 6-month arrhythmia burden in relation to LVAD implantation and VA ablation.A total of 9 patients underwent both LVAD implantation and VA ablation. There were 3 and 6 patients, respectively, in the pre-LVAD and post-LVAD cohorts. Among patients in the pre-LVAD cohort, the median number of VAs tended to increase after ablation (9 vs. 72) and decreased after LVAD implantation (72 vs. 63). Similarly among patients in the post-LVAD cohort, the median burden of VAs increased after LVAD implantation (1 vs. 22) and the median burden decreased after ablation (22 vs. 13). Two of 6 patients had substrate related to the LVAD inflow cannula site, while other substrate was not related directly to the cannula.In patients with progressive HF and LVAD implantation, ablation is associated with reduced VA rates. In LVAD patients, most VAs arise from substrate unrelated to the inflow cannula site.

Resident in Internal Medicine, Mayo School of Graduate Medical Education, Rochester, MN (C.T.L., Y.N.R.); Advisor to residents and Consultant in Cardiovascular Diseases, Mayo Clinic, Rochester, MN (C.R.B.). A 62-year-old woman presented to the emergency department after a mechanical fall onto her left hip. She had been in her usual state of health earlier that day, but after the fall she experienced intractable leg pain and was unable to bear weight on her left hip. She reported no chest pain, dyspnea, palpitations, light-headedness, or dizziness before the event. Her medical history was notable for hypertension and nicotine and alcohol dependence. Her initial physical examination revealed evidence of severe left hip tenderness and pain with motion. The remainder of her examination findings were unremarkable. Radiography of the left hip revealed a left intertrochanteric hip fracture with minimal displacement. She underwent prompt surgical repair with internal fixation using a cephalomedullary nail. The patient tolerated the procedure well with no complications and minimal blood loss. Postoperatively, she received deep venous thrombosis prophylaxis with subcutaneous heparin. Her pain subsided considerably after the operation. At 36 hours postoperatively, the patient experienced sudden shortness of breath with severe respiratory distress. On examination, she was somnolent and had a blood pressure of 90/54 mm Hg and a heart rate of 131 beats/min. She was tachypneic (respiratory rate, 20 breaths/min) and hypoxic (oxygen saturation, 90% with a face mask delivering 40% fraction of inspired oxygen). The patient was afebrile and drowsy but was able to follow commands. Cardiac examination revealed a right ventricular (RV) precordial heave, elevated jugular venous pressure, and cool extremities with a weakly palpable pulse. Auscultation identified a right-sided third heart sound but no murmurs. Lung examination revealed diffuse bilateral crackles but no decreased breath sounds at the base or dullness to percussion suggestive of a pleural effusion. She had bilateral mild pitting edema on the lower

Kidney transplant recipients may develop new-onset diabetes after transplantation (NODAT) and transplant-associated hyperglycemia (TAH) (NODAT or new-onset impaired glucose tolerance-IGT). We studied 251 consecutive renal transplant South Asian recipients for incidence of NODAT and its risk factors between June 2004 and January 2009. Pre-transplant glucose tolerance test (GTT) identified non-diabetics (n = 102, IGT-24, NGT-78) for analysis. Baseline immunosuppression along with either cyclosporine (CsA) (n = 70) or tacrolimus (Tac) (n = 32) was given. Patients underwent GTT 20 days (mean) post-transplant to identify NODAT, normal (N) or IGT. TAH was observed in 40.2% of the patients (40% in CsA and 40.6% in Tac) (P = 0.5). NODAT developed in 13.7% of the patients (12.9% in CsA and 15.6% in Tac) (P = 0.5). Overall, Hepatitis C (P = 0.007), human leukocyte antigen (HLA) B52 (P = 0.03) and lack of HLA A28 (A68/69) (P = 0.03) were associated with TAH. In the Tac group, higher Day 1 dosage (P

The aim of this study was to assess incidence and risk factors for acute kidney injury (AKI) in patients with dengue fever (DF). A total of 223 patients (males, 130; females, 93; mean age, 26.2 ± 18.2 years) from a tertiary care centre in southern India were retrospectively analysed. Acute renal failure (ARF) developed in 24 (10.8%) patients. Based on the Acute Kidney Injury Network (AKIN) criteria, the results revealed that: 12 (5.4%) had mild AKI; seven (3.1%) had moderate AKI; and five (2.2%) had severe AKI. A further 54 (24%) were diagnosed with dengue haemorrhagic fever (DHF); 11 (5%) were co-infected with leptospirosis; thrombocytopenia was present in 157 (70%); and 64 (29%) were hypotensive. Patients were divided into either group A (with AKI) or group B (without AKI), and group A was divided into mild (A1), moderate (A2) and severe (A3) subgroups. We recorded: a higher total white count (A = 9824; B = 6706; P = 0.01); serum glutamic pyruvic transaminase (SGPT; A = 450; B = 144; P = 0.001); alkaline phosphatase (ALP) levels (A = 207; B = 42; P = 0.001); lower albumin (A = 2.65; B = 3.09; P < 0.001); and serum bicarbonate (A = 20.57; B = 23.21; P = 0.009). Hypotension ( P = 0.01), coexisting viral hepatitis ( P < 0.001), sepsis ( P < 0.001), multiple organ dysfunction syndrome (MODS; P < 0.001) and the need for inotropes ( P < 0.001) were associated with DF. Total white count ( P = 0.038), glomerular filtration rate (GFR) on discharge ( P = 0.034), specific gravity of urine ( P = 0.006), ALP ( P = 0.013), SGPT ( P = 0.042), MODS ( P = 0.05) and use of platelet fresh frozen plasma (FFP; P = 0.007) were significantly different between mild, moderate and severe AKI subgroups. Twenty-two (9%) died. AKI is associated with an increased mortality in DF ( P = 0.005).

Only 3–5% of all patients with end-stage renal disease (ESRD) in India get some form of RRT from the existing pool of 900 nephrologists [2, 3]. As referral pattern varies widely in India for uremia therapy, there is no robust national database on the prevalence and incidence of dialysis therapy except for isolated reports. The cost of maintenance hemodialysis (MHD) for a single session varies from US $10 to 65 and most patients are maintained on twice-aweek dialysis. One-third of the 30 000 MHD patients are in the major metropolitan cities of Chennai, Delhi, Mumbai and Kolkata, whereas the majority of the Indian population lives in small towns and villages far away from cities. The hidden cost of travel to the hemodialysis (HD) center and loss of daily wages for the patient and the accompanying person is not usually calculated when the cost of HD is taken into consideration. The unmet needs of RRT must be covered by continuous ambulatory peritoneal dialysis (CAPD) that is available even in remote places in the country. There are ~7000 prevalent patients on chronic peritoneal dialysis in India. The cost is substantially less with PD, and the four industries which are involved in CAPD in India have network systems to deliver dialysis supplies to the residence without any additional cost. The use of erythropoietin (EPO) and iron is comparatively lower in CAPD patients compared to HD patients in India to the advantage of CAPD as a favorable RRT.

AIM To perform a systematic-review and meta-analysis to compare outcomes of ivabradine combined with beta-blocker to beta-blocker alone in heart failure with reduced ejection fraction (HFrEF). METHODS We searched PubMed, Cochrane, EMBASE, CINAHL and Web of Science for trials comparing ivabradine + beta-blocker to beta-blocker alone in HFrEF. We performed a systematic-review and meta-analysis of published literature. Primary end-point was combined end point of cardiac death and hospitalization for heart failure. RESULTS Six studies with 17671 patients were included. Mean follow-up was 8.7 ± 7.9 mo. Combined end-point of heart failure readmission and cardiovascular death was better in ivabradine + beta-blocker group compared to beta-blocker alone (RR: 0.93, 95%CI: 0.79-1.09, P = 0.354). Mean difference (MD) in heart rate was higher in the ivabradine + beta-blocker group (MD: 6.14, 95%CI: 3.80-8.48, P < 0.001). There was no difference in all cause mortality (RR: 0.98, 95%CI: 0.89-1.07, P = 0.609), cardiovascular mortality (RR: 0.99, 95%CI: 0.86-1.15, P = 0.908) or heart failure hospitalization (RR: 0.87, 95%CI: 0.68-1.11, P = 0.271). CONCLUSION From the available clinical trials, ivabradine + beta-blocker resulted in a significantly greater reduction in HR coupled with improvement in combined end-point of heart failure readmission and cardiovascular death but with no improvement in all cause or cardiovascular mortality. Given the limited evidence, further randomized controlled trials are essential before widespread clinical application of ivabradine + beta-blocker is advocated for HFrEF.

A 57-year-old woman with a creatinine of 0.8 mg/dL and a normal urine analysis, was investigated with technetium-99m renogram and multidetector computerized tomography (MDCT) as a renal donor for her daughter. The glomerular filtration rate (GFR) was 100 mL/min with the left kidney 42 mL/min and right kidney 58 mL/ min. MDCT revealed a large lipomatous tumour on the renal cortex of the left lower pole with exophytic extension into the perirenal space measuring 7.3 3 5.2 cm (Figure 1). The arterial phase revealed dual arterial supply to the left kidney with the tumour being supplied by a branch from the lower renal artery (Figure 2a). The presence of fat [67 Hounsfield unit (HU)] with interposed soft tissue (42 HU), ectatic vessels and an aneurysm that measured 9 mm 3 8.9 mm with no direct arteriovenous shunting favoured the diagnosis of angiomyolipoma. Superselective catheterization of the feeding artery was performed and the neovascular vessels were embolized. Post-embolization MDCT revealed complete obliteration of the abnormal feeding artery and the aneurysmal lumen (Figure 2b). A week later, the GFR was 107 mL/min, left kidney 43 mL/min and right kidney 64 mL/min. Angiomyolipoma is a benign renal neoplasm with variable amounts of fat, vascular and smooth muscle elements. Attenuation of less than 20 HU on computerized tomography is widely accepted to confirm the presence of fat and this finding confirms the diagnosis of angiomyolipoma [1]. A tumour >4 cm with an aneurysm measuring >5 mm has a high risk of rupture [2].