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AIMS: Comprehensive echocardiography assessment of right ventricular (RV) impairment has not been reported in critically ill patients with COVID-19. We detail the specific phenotype and clinical associations of RV impairment in COVID-19 acute respiratory distress syndrome (ARDS). METHODS: Transthoracic echocardiography (TTE) measures of RV function were collected in critically unwell patients for associations with clinical, ventilatory and laboratory data. RESULTS: Ninety patients (25.6% female), mean age 52.0 ± 10.8 years, veno-venous extracorporeal membrane oxygenation (VVECMO) (42.2%) were studied. A significantly higher proportion of patients were identified as having RV dysfunction by RV fractional area change (FAC) (72.0%,95% confidence interval (CI) 61.0-81.0) and RV velocity time integral (VTI) (86.4%, 95 CI 77.3-93.2) than by tricuspid annular plane systolic excursion (TAPSE) (23.8%, 95 CI 16.0-33.9), RVS' (11.9%, 95% CI 6.6-20.5) or RV free wall strain (FWS) (35.3%, 95% CI 23.6-49.0). RV VTI correlated strongly with RV FAC (p ≤ 0.01). Multivariate regression demonstrated independent associations of RV FAC with NTpro-BNP and PVR. RV-PA coupling correlated with PVR (univariate p

Background Coronary microvascular dysfunction is prevalent in chronic kidney disease (CKD), and may contribute to the development of myocardial dysfunction in CKD. Coronary flow velocity reserve (CFVR) is a marker of coronary microvascular function and falls with increasing CKD stage. Living kidney donors have renal function consistent with early stage CKD and concern has been raised about their cardiovascular risk. No studies to date have investigated the presence of coronary microvascular dysfunction in living kidney donors. Methods 25 healthy controls and 23 living kidney donors were recruited and underwent assessment with transthoracic echocardiography, Doppler CFVR, myocardial contrast echocardiography and serum multiplex immunoassay panels. Results Doppler CFVR was significantly reduced in living kidney donors compared to controls (mean CFVR 3.4 ± 0.7 vs 3.8 ± 0.6, mean difference 0.4 95% confidence interval 0.03–0.8, p =.036). Quantitative myocardial contrast echocardiography showed a trend towards reduced coronary flow reserve in living kidney donors. Compared to controls, living kidney donors had higher serum high sensitivity C reactive peptide (hsCRP) and lower levels of uromodulin. Conclusions This is the first study of CFVR in living kidney donors. We have shown that the modest drop in estimated glomerular filtration rate in living kidney donors is associated with lower values of Doppler CFVR compared to controls, suggesting that isolated reductions in renal function may lead to altered microvascular function. The increase in hsCRP and reduction in uromodulin suggests that chronic subclinical inflammation may contribute to altered microvascular function in this population., Highlights • Coronary flow velocity reserve is reduced in living kidney donors compared to controls. • Markers of inflammation are elevated in living kidney donors. • Inflammation may cause coronary microvascular dysfunction in living kidney donors. • Living kidney donors need aggressive cardiovascular risk factor management.

Aims To assess the clinical effectiveness of a sonographer-led, cardiologist-interpreted stress echocardiography (SE) service in a rapid access stable chest pain clinic (RACPC) setting. Methods and results Baseline data was collected prospectively on 768 consecutive patients, referred from the RACPC, who underwent SE between May 2014 and May 2015. Retrospective analysis was performed on follow-up data for outcomes. Among 768 patients (mean age 58 years, 57.8% males) with a mean pre-test probability of coronary artery disease (CAD) of 31%, 675 (88%) underwent SE on the same day as the RACPC consultation. Diagnostic tests were obtained in 749 (97.5%) cases with 62 (8.1%) demonstrating inducible ischemia. Coronary angiography was performed in 61 patients of whom 54 demonstrated flow-limiting CAD (positive predictive value: 88.5%). There was no occurrence of serious adverse events. During a mean follow-up period of 2.5 years, 20 first cardiac events were recorded, of which annualised events in the normal SE group were 0.64% versus 5.8% in patients with an abnormal SE (log rank p Conclusion Sonographer-led SE interpreted by a cardiologist is feasible, safe and efficacious. It impacted on the management of patients with appropriate outcomes and may be a cost-efficient and safer alternative to other non-invasive imaging modalities in the RACPC setting.

Measures of left ventricular (LV) systolic and diastolic function are known predictors of mortality after repair of tetralogy of Fallot. We aimed to characterise LV reverse remodelling achievable with ramipril therapy.A blinded post-hoc analysis of baseline and 6-month follow-up echocardiograms from the APPROPRIATE (ISRCTN: 97515585) randomised double-blinded placebo-controlled trial of ramipril therapy was performed in 64 patients: 32 in ramipril and 32 in placebo group. Tissue Doppler systolic and diastolic myocardial velocities, mitral inflow velocities and time intervals were measured. Left atrial area and left atrial emptying fraction were calculated. There was significant increase in long axis shortening mean (standard deviation); MAPSE [1.9 (4.2) mm vs -0.2 (3.7) mm; p = 0.030], peak lateral systolic velocity; S' lateral [1.0 (2.0) cm/s vs -0.3 (2.2) cm/s; p = 0.025], peak lateral early diastolic velocity; E' lateral [0.57 (2.4) cm/s vs -3.3 (3.9) cm/s; p 0.001], transmitral to lateral mitral annular early diastolic velocity ratio; E/E' lateral [-0.7 (1.9) vs 1.5 (1.9); p 0.001] over the study period in the ramipril compared to the placebo group. Significantly higher measurements were observed in the ramipril arm of the subgroup of patients with right ventricular restrictive physiology in terms of peak late diastolic velocity; A [5.9 (13.5) cm/s vs -5.8 (12.5) cm/s; p = 0.041] and early to late diastolic transmitral velocity ratio; E/A [-0.18 (0.42) vs 0.23 (0.48); p = 0.037].Six months' ramipril treatment appears to limit progression of both diastolic and systolic LV function in adults late after tetralogy of Fallot repair. With increased appreciation that even subtle LV disease predicts tetralogy of Fallot outcomes, further clinical trials of drug therapies are justified.

Introduction Exercise ECG (Ex-ECG) is advocated by guidelines for patients with low - intermediate probability of coronary artery disease (CAD). However, there are no randomized studies comparing Ex-ECG with exercise stress echocardiography (ESE) evaluating long term cost-effectiveness of each management strategy. Methods Accordingly, 385 patients with no prior CAD and low-intermediate probability of CAD (mean pre-test probability 34%), were randomized to undergo either Ex-ECG (194 patients) or ESE (191 patients). The primary endpoint was clinical effectiveness defined as the positive predictive value (PPV) for the detection of CAD of each test. Cost-effectiveness was derived using the cumulative costs incurred by each diagnostic strategy during a mean of follow up of 3.0 years. Results The PPV of ESE and Ex-ECG were 100% and 64% (p = 0.04) respectively for the detection of CAD. There were fewer clinic (31 vs 59, p 20% reduction in cost with an ESE strategy with no difference in the combined end-point of death, myocardial infarction, unplanned revascularization and hospitalization for chest pain between ESE and Ex-ECG (3.2% vs 3.7%, p = 0.38). Conclusion In patients with low to intermediate pretest probability of CAD and suspected angina, an ESE management strategy is cost-effective when compared with Ex-ECG during long term follow up.

BACKGROUND: Although calcific aortic valve disease (CAVD) is associated with coronary atherosclerosis, it is not known whether early CAVD is associated with coronary microcirculatory dysfunction (CMD). We sought to investigate the relationship between myocardial blood flow reserve (MBFR) - a measure of CMD, and early CAVD in the absence of obstructive epicardial coronary artery disease. We also determined whether this relationship was independent of coronary artery disease (CAD) and hs-CRP, a marker of systemic inflammation. METHODS: 183 patients with chest pain and unobstructed coronary arteries were studied. Aortic valve calcification score (AVCS), coronary total plaque length (TPL), and coronary calcium score were quantified from multislice CT. MBFR was assessed using vasodilator myocardial contrast echocardiography. Hs-CRP was measured from venous blood using a particle-enhanced immunoassay. RESULTS: Mean (±SD) participant age was 59.8 (9.6) years. Mean AVCS was 68 (258) AU, TPL was 15.6 (22.2) mm, and median coronary calcification score was 43.5AU. Mean MBFR was 2.20 (0.52). Mean hs-CRP was 2.52 (3.86) mg/l. Multivariable linear regression modelling incorporating demographics, coronary plaque characteristics, MBFR, and inflammatory markers, demonstrated that age (β=0.05, 95% CI: 0.02, 0.08, P=0.007), hs-CRP (β=0.09, CI: 0.02, 0.16, P=0.010) and diabetes (β=1.03, CI: 0.08, 1.98, P=0.033), were positively associated with AVCS. MBFR (β=-0.87, CI: -1.44, -0.30, P=0.003), BMI (β=-0.11, CI: -0.21, -0.01, P=0.033), and LDL (β=-0.32, CI: -0.61, -0.03, P=0.029) were negatively associated with AVCS. TPL and coronary calcium score were not independently associated with AVCS when included in the regression model. CONCLUSION: Coronary microvascular function as determined by measurement of myocardial blood flow reserve is independently associated with early CAVD. This effect is independent of the presence of coronary artery disease and also systemic inflammation.

Background Atrial fibrillation (AF) ablation procedures are increasingly being performed in patients receiving direct oral anticoagulants (DOACs). Experience regarding the safety of edoxaban in this context is limited. In an exploratory analysis we therefore investigated the outcome of patients undergoing transcatheter AF ablation in the ENGAGE AF-TIMI 48 trial. Methods & results During the trial, 193 transcatheter AF ablation procedures were performed in 169 patients. For the majority of ablations (n=157, 81%), study drug was interrupted >3days (median time of interruption: 18days, interquartile range 3–30days); 86 ablations were performed with ≤10days, and 36 ablations with ≤3days study drug interruption. During the first 30days after the ablation, one ischemic stroke was observed in the warfarin group and none in the higher-dose edoxaban regimen (HDER) or lower-dose edoxaban regimen (LDER) group. Three clinically relevant non-major (CRNM) bleeding events were observed in the warfarin group; one major bleed was seen in the HDER group; one minor bleed occurred in the LDER group. All bleeding events occurred among the patients with ≤10days study drug interruption; in contrast, no ischemic events or deaths were observed in these patients. Conclusions In this pilot evaluation of the ENGAGE AF-TIMI 48 trial, treatment with edoxaban was associated with a low risk of ischemic and bleeding events during the first 30days post ablation.

Hypoglycaemia is associated with increased cardiovascular and all-cause mortality in both subjects with and without coronary artery disease (CAD) [1]. Our group recently demonstrated that insulin-induced hypoglycaemia (IIH) is associated with a 14% reduction of myocardial blood flow reserve (MBFR) compared to baseline, in both healthy subjects and those with type 1 diabetes mellitus (T1DM) [2]. Cardiac troponin is a sensitive marker of myocardial injury and higher levels have been linked to adverse outcomes in patients with ACS [3]. A new ultrasensitive cardiac troponin I (us-cTnI) has been developed which has a limit of detection of at least one order of magnitude lower below that of current commercial assays. In comparison with current generation troponin assays, us-cTnI has been shown to be more sensitive in the detection of myocardial ischaemia. Furthermore, low but elevated levels of us-cTnI in patients presenting with suspected ACS, have been linked to adverse cardiovascular outcomes and death [4]. This study investigated whether 60 min duration of symptomatic IIH and reduction in MBFR, was associated with myocardial injury as determined by a change in serum levels of us-cTnI measured immediately following hypoglycaemia, in healthy and diabetic subjects without obstructive CAD.

Following ST elevation acute myocardial infarction (STEMI) and reperfusion therapy, there are often persistent wall thickening (WT) abnormalities and perfusion defects due to variable degree of myocardial stunning and necrosis. We hypothesised that following STEMI and reperfusion therapy, the extent of residual perfusion assessed by myocardial contrast echocardiography (MCE) and not the extent of WT abnormalities would predict subsequent global recovery of left ventricular (LV) function.Accordingly, 112 patients with STEMI underwent simultaneous assessment of WT abnormality and perfusion using MCE 7+/-2 days after AMI and reperfusion therapy. Both WT and perfusion were scored on a 16 segment LV model. Contrast perfusion index (CPI), and global LV function were calculated. Echocardiography was repeated 12 weeks after reperfusion to assess recovery of LV function.Of the 112 patients recruited, follow up echocardiography 12 weeks after reperfusion was available in 98 patients. CPI was significantly higher (p0.0001) in the 66 patients, who showed late recovery of LV function (1.67+/-0.27) compared to those who did not show recovery of function (1.25+/-0.04). No significant difference was noted in the indices of baseline LV function in patients with (1.67+/-0.32) and without (1.80+/-0.36) recovery of LV function. The multivariable predictors of late recovery of function were MCE (p=0.02), absence of diabetes (p=0.02) and lower peak creatine kinase (p=0.01).The extent of residual contrast perfusion and not WT abnormalities predicts late recovery of global LV function after acute myocardial infarction and reperfusion therapy.

Dear EditorIt is known that judging the severity of aortic stenosis (AS) in pa-tients with co-existent left ventricular (LV) systolic dysfunction can bechallenging. These patients are particularly difficult for the managingclinicianastheir operativeriskis high butoutcomewith medical thera-py is poor. Quantitative Doppler echocardiography permits calculationof the aortic valve area (AVA), which may be b1.0 cm

Mild to moderate renal impairment (MMRI) is associated with an excess cardiovascular mortality but the reason for this is unclear. Increased left ventricular mass (LVM) is associated with severe renal dysfunction and a higher cardiovascular mortality. However, whether increased LVM also occurs in patients with milder renal dysfunction is unknown.336 consecutive patients under investigation for chest pain who underwent concurrent coronary angiography, serum creatinine (Cr) and LVM assessment, were recruited from a university hospital in Shanghai, China. The main outcome measures were: LVM normalised for body surface area (NLVM), renal function determined by Cr, creatinine clearance (CrCl) (Cockroft-Gault equation) and glomerular filtration rate (GFR) (Modification of Diet in Renal Disease equation).Mean+/-SD age was 56.8+/-9.5 years, 282 (84%) were male, mean NLVM 107.1+/-36.8 g/m(2), Cr 0.94+/-0.22 mg/dL, CrCl 82.7+/-21.7 mL/min/1.73 m(2) and GFR 89.4+/-24.6 mL/min/1.73 m(2). NLVM was related to Cr (r=-0.30), CrCl (r=0.19) and GFR (r=0.24) (all p0.001). A multiple logistic regression model using quartile analysis of renal function showed that those patients with a Cr 1.06-2.00 mg/dL, CrCl 34.8-67.5 mL/min/1.73 m(2) and a GFR 36.2-73.4 mL/min/1.73 m(2) were significantly associated with increased NLVM, independent of other variables. Using definitions derived from the National Kidney Foundation Guidelines multiple regression analysis showed MMRI to be independently associated with increased NLVM: Cr 1.2-1.9 mg/dL, odds ratio (OR) 2.77 (CI 1.04-7.40) (p=0.04); CrCl 30-89.9 mL/min/1.73 m(2), OR 1.63 (CI 0.91-2.93) (p=0.11); GFR 30-89.9 mL/min/1.73 m(2), OR 1.76 (CI 1.07-2.90) (p=0.03).In patients being investigated for chest pain, MMRI is significantly and independently associated with increased LVM.

Takotsubo cardiomyopathy (TC) is a recognised cause of reversible left ventricular (LV) dysfunction. It has attracted considerable attention in recent years since its presentation frequently mimics that of ST-segment elevation myocardial infarction. The exact aetiology remains ill-defined, although stress is often a precipitating factor. Recently it has emerged that stress testing can also induce TC. We report a case of TC during pharmacological (dobutamine) but not physiological (treadmill) stress echocardiography (SE) in the same patient and explore possible pathophysiological explanations for this observation. A 71 year old lady was referred for SE to investigate chronic exertional dyspnoea. She suffered from hypertension but had no other medical history. Resting echocardiography revealed mild concentric LV hypertrophy, a dilated left atrium (dimension 5.0 cm) and normal LV systolic function (biplane EF 66%). There was no significant valvular disease or pulmonary hypertension. A recent knee injury prevented exercise and thus she underwent dobutamine echocardiography (DbE) using a standard ischaemia protocol (dobutamine infused peripherally in 3-minute dose increments, starting from 10 μg/kg/min and increasing to 20, 30 and finally 40 μg/kg/min). Peak heart rate was 142 bpm (96% age-predicted maximum), peak BP 169/80 mm Hg and rate-pressure product 24140. Peak stress imaging revealed new dilatation and ballooning of the LV apex with normal contractility of the basal segments (Fig. 1A and B and online movie clip 1). One minute after ceasing dobutamine infusion, she complained of dizziness and her blood pressure fell to 94/ 50 mm Hg. Spectral (continuous wave) doppler imaging revealed significant left ventricular outflow tract obstruction (LVOTO) of almost 120 mm Hg (Fig. 1C). She did not experience chest pain and, interestingly, did not have any ischaemic ECG changes. She recovered over the next 10 min with rest and oral fluids and was allowed to go home with a plan to return for exercise SE, as the sequence of events and imaging appearances were highly suggestive of dobutamineinduced TCwith associated LVOTO rather than coronary artery disease. She returned 3 months later, once her knee had improved, and performed treadmill exercise SE. She was able to walk for 6 min and achieved similar maximum heart rate (146 bpm, 98% age-predicted maximum), blood pressure (170/70 mm Hg) and rate-pressure product (24674) to the first SE study. On this occasion, normal contractility was seen in all segments with no apical ballooning and no LVOT obstruction (Fig. 2A, B and C and online movie clip 2). The patient was reassured and has been well during follow-up. She returned 3 months later, once her knee had improved, and performed treadmill exercise SE. She was able to walk for 6 min and achieved similar maximum heart rate (146 bpm, 98% age-predicted maximum), blood pressure (170/70 mmHg) and rate-pressure product (24674) to the first SE study. On this occasion, normal contractility was seen in all segments with no apical ballooning and no LVOT obstruction (Fig. 2A, B and C and online movie clip 2). The patient was reassured and has been well during follow-up. TC is a reversible form of myocardial dysfunction, classically seen after sudden severe emotional or physical stress and of immediate clinical priority as the ECG frequently shows ST segment elevation. TC is a recognised cause of systolic anterior motion (SAM) of the mitral valve and LVOTO, which complicates up to 10% of TC cases [1]. TC, both with [2] and without [3] SAM and LVOTO, has been described during DbE though the incidence is unknown. The exact pathophysiological basis of TC remains incompletely understood, although catecholamine excess is widely accepted as a probable contributing factor. In thewesternworld, the vast majority of cases are seen in post-menopausal women, suggesting a hormonal role in the pathogenesis. Previous studies have also found that

Patients with pathological left ventricular hypertrophy have depressed midwall systolic shortening in spite of normal indices of left ventricular chamber function and a reduced midwall function has been observed to be an independent predictor of cardiovascular risk. Whether midwall shortening is depressed in physiological hypertrophy is unknown.Forty-two subjects, 27 athletes and 15 age- and sex-matched normal control subjects (group 1) were studied. The athletes were divided into those with eccentric hypertrophy (group 2) and those with concentric hypertrophy (group 3). Systolic left ventricular function was assessed at the midwall and endocardium using two-dimensional echocardiography in all subjects.Left ventricular mass index was significantly greater in both athletic groups than in controls (group 1, 101+/-5.8 g/m(2), group 2, 141+/-11.1*, group 3, 155+/-5.8*; *P0.01 compared with group 1). Left ventricular systolic function assessed at the endocardium was similar among all three groups (ejection fraction: group 1, 66.2+/-2.38, group 2, 66.8+/-1.44, group 3, 63.7+/-1.66%; endocardial fractional shortening: group 1, 37.1+/-1.71, group 2, 37.6+/-1.13, group 3, 35.1+/-1.25%). However, fractional shortening at the midwall was reduced in the concentric hypertrophy athletes compared with the other two groups (midwall fractional shortening: group 1, 21.9+/-1.1, group 2, 21.9+/-0.86, group 3, 18.4+/-0.96*%; P0.05 compared with groups 1 and 2).Subjects with physiological concentric hypertrophy have depressed midwall fractional shortening. This suggests that the observed discrepancy between midwall and endocardial shortening in patients with left ventricular hypertrophy is likely to be a function of the geometry and not necessarily a reflection of pathology within the myocardium.

Aims : To determine the prognostic value of a normal stress echocardiogram in the setting of a large district general nonuniversity hospital in the United Kingdom. Methods : Between January 1996 and December 1999, all patients who had undergone stress echocardiography were identified and those with normal results were studied. Normal stress echocardiograms were found in 252 patients, 19 of whom were lost to follow-up. Deaths and nonfatal myocardial infarctions were considered hard cardiac events and data was collected in the remaining 233 patients. Results : Among the 233 patients, the pre-test probability of coronary artery disease was low in 68 (27.9%) and intermediate or high in 168 (72.1%). During a follow-up period of mean (SD) 2.7 (1.1) years, death occurred in 4 patients of which 3 were consequent to acute myocardial infarctions and 1 was unexplained. One patient sustained a nonfatal infarction. Thus, the annualized mortality and hard event rates were 0.6% per patient/year and 0.8% per patient/year, respectively. Conclusions : A normal stress echocardiogram portends an excellent prognosis, even in a cohort with a high proportion of patients having intermediate or high pre-test probability of coronary artery disease.

To delineate the natural history of left ventricular remodelling following large anterior myocardial infarction (MI), in the era of aggressive medical therapy.Seventeen selected patients underwent cardiovascular magnetic resonance (CMR) at 2 weeks and 1, 3, 6 and 12 months post infarction.There was a significant increase in left ventricular (LV) end-diastolic volume index (EDVI) and LV ESVI from 2 weeks to 1 month (P0.05) but no significant change thereafter. The LV ejection fraction (EF) decreased from 2 weeks to 1 month (P0.05) and then increased over the year (P=0.02). Throughout the study period the sphericity index increased. There was a significant and progressive decrease in LV mass index over the year, which was associated with a decrease in wall thickness at both the infarct and non-infarct sites. Independent predictors of an early increase in LVESVI were increasing age, increasing CK-MB and not receiving treatment with a statin.This study delineates the natural history of left ventricular remodelling in the modern medical era in those patients who have suffered a large anterior MI. Classical remodelling occurred up to 1 month, but thereafter was attenuated. These findings would suggest that remodelling is not as prevalent in the modern era, and that combined medical management with thrombolysis, ACEi, beta-blockers and statins may strongly influence the development of this remodelling.

Background Controversy exists regarding the significance of pathological ‘Q' waves on electrocardiography (ECG) following established acute myocardial infarction (AMI) in predicting non-viable myocardium. Aim The aim of the study was to ascertain the reliability of ‘Q' waves on ECG to predict myocardial viability following AMI. Methods 176 patients underwent both ECG and DSE, at a mean of 4.9days post AMI. Non-viability on ECG and DSE was defined as mentioned below. Both ECG and DSE were used to evaluate 352 (176 anterior and 176 inferior) myocardial territories for viability. Results The positive predictive value and the negative predictive value of ‘Q' waves on ECG to predict non-viable myocardium were 43% and 85% respectively. The sensitivity for ECG to detect non-viable myocardium was rather low for both anterior and inferior ‘Q' waves (64% and 65% respectively), and, the specificity was as well not high enough (72% for anterior and 69% for inferior). Conclusion The presence of extensive ‘Q' waves does not predict non-viable myocardium. Whereupon, absence of ‘Q' waves predicts the presence of viable myocardium for inferior territory but this is relatively less reliable for anterior territory. Myocardial viability should be sought in patients with extensive ‘Q' waves and in unclear anterior territories.

Myocardial uptake using 99m Tc-sestamibi single photon emission computed tomography (SPECT) depends largely on myocardial microvascular volume. Myocardial contrast echocardiography (MCE) is a relatively new technique that detects not only microvascular volume but also blood flow. These differing mechanisms may affect the relative accuracies of MCE and SPECT for detecting myocardial viability (MV) early after acute myocardial infarction (AMI) and thrombolysis. Accordingly 56 patients underwent resting transthoracic echocardiography, low-power MCE and SPECT 7±2 days following first AMI and thrombolysis. Contractile reserve (CR) was assessed 3 months following revascularization. The sensitivity and specificity of MCE and SPECT were 83% and 78% ( p =ns) and 78% and 45% ( p p =0.01). The different physiological mechanisms employed by MCE and SPECT translate into different relative accuracies for the detection of MV.

To compare electrocardiogram (ECG) with measurement of N-terminal pro-B-type natriuretic peptides (NTproBNP) as the General Practitioner's (GP) initial test for suspected heart failure patients from the community. We prospectively studied 137 suspected heart failure patients who underwent ECG and NTproBNP estimation; were referred from primary care to a specialist unit for echocardiography. We demonstrated that sensitivity of ECG interpreted by GP was significantly lower than both by ECG interpreted by Hospital Physician (HP) and NTproBNP estimation for the detection of left ventricular systolic dysfunction (LVSD). Therefore, measurement of NTproBNP is a better investigation in primary care than ECG for the detection of significant LVSD.