Noncardiac Dyspnea Research Articles

Heart failure with preserved ejection fraction or non-cardiac dyspnea in paroxysmal atrial fibrillation: The role of left atrial strain

BackgroundDiagnosis of heart failure with preserved ejection fraction (HFpEF) in patients with dyspnea and paroxysmal atrial fibrillation (AF) is challenging. Speckle tracking-derived left atrial strain (LAS) provides an accurate estimate of left ventricular (LV) filling pressures and left atrial (LA) phasic function. However, data on clinical utility of LAS in patients with dyspnea and AF are scarce. ObjectiveTo assess relationship between the LAS and the probability of HFpEF in patients with dyspnea and paroxysmal AF. MethodsThe study included 205 consecutive patients (62 ± 10 years, 58% males) with dyspnea (NYHA≥II), paroxysmal AF and preserved LV ejection fraction (≥50%), who underwent speckle tracking echocardiography during sinus rhythm. Probability of HFpEF was estimated using H2FPEF and HFA-PEFF scores, which combine clinical characteristics, echocardiographic parameters and natriuretic peptides. ResultsPatients with high probability of HFpEF were significantly older, had higher body mass index, NT-proBNP, E/e’, pulmonary artery pressure and larger LA volume index than patients in low-to-intermediate probability groups (all p < 0.05). All components of LAS and LA strain rate showed proportional impairment with increasing probability of HFpEF (all p < 0.05). Out of the speckle tracking-derived parameters, reservoir LAS showed the largest area under the curve (AUC = 0.78, p < 0.001) and the strongest independent predictive value (OR: 1.22, 95% CI 1.08–1.38) to identify patients with high probability of HFpEF. ConclusionsReservoir LAS shows a high diagnostic performance to distinguish HFpEF from non-cardiac causes of dyspnea in symptomatic patients with paroxysmal AF.

Diagnostic and prognostic values of the QRS-T angle in patients with suspected acute decompensated heart failure.

AimsThe aim of this study was to investigate the diagnostic and prognostic utility of the QRS‐T angle, an electrocardiogram (ECG) marker quantifying depolarization–repolarization heterogeneity, in patients with suspected acute decompensated heart failure (ADHF).Methods and resultsWe prospectively enrolled unselected patients presenting to the emergency department with symptoms suggestive of ADHF. The QRS‐T angle was automatically derived from a standard 12‐lead ECG recorded at presentation. The primary diagnostic endpoint was a final adjudicated diagnosis of ADHF. The primary prognostic endpoint was all‐cause mortality during 2 years of follow‐up. Among the 1915 patients enrolled, those with higher QRS‐T angles were older, were more commonly male, and had a higher rate of co‐morbidities such as arterial hypertension, coronary artery disease, or chronic kidney disease. ADHF was the final adjudicated diagnosis in 1140 (60%) patients. The QRS‐T angle in patients with ADHF was significantly larger than in patients with non‐cardiac causes of dyspnoea {median 110° [inter‐quartile range (IQR) 46–156°] vs. median 33° [IQR 15–57°], P < 0.001}. The diagnostic accuracy of the QRS‐T angle as quantified by the area under the receiver operating characteristic curve (AUC) was 0.75 [95% confidence interval (CI) 0.73–0.77, P < 0.001], which was inferior to N‐terminal pro‐B‐type natriuretic peptide (AUC 0.93, 95% CI 0.92–0.94, P < 0.001), but similar to that of high‐sensitivity troponin T (AUC 0.78, 95% CI 0.76–0.80, P = 0.09). The AUC of the QRS‐T angle for discrimination between ADHF and non‐cardiac dyspnoea remained similarly high in subgroups of patients known to be diagnostically challenging, including patients older than 75 years [0.71 (95% CI 0.67–0.74)], renal failure [0.79 (95% CI 0.71–0.87)], and atrial fibrillation at presentation [0.68 (95% CI 0.60–0.76)]. Mortality rates according to QRS‐T angle tertiles were 4%, 6%, and 10% after 30 days (P < 0.001) and 24%, 31%, and 43% after 2 years (P < 0.001). After adjustment for clinical, laboratory, and ECG parameters, the QRS‐T angle remained an independent predictor for 2 year mortality with a 4% increase in mortality for every 20° increase in QRS‐T angle (P = 0.02).ConclusionsThe QRS‐T angle is a readily available and inexpensive marker that can assist in the discrimination between ADHF and non‐cardiac causes of acute dyspnoea and may aid in the risk stratification of these patients.

Diagnosis and treatment strategy of coronavirus disease 2019 with cardiovascular disease in elderly patients.

Diagnosis and treatment strategy of coronavirus disease 2019 with cardiovascular disease in elderly patients.

Central role of left atrial dynamics in limiting exercise cardiac output increase and oxygen uptake in heart failure: insights by cardiopulmonary imaging.

In heart failure (HF), the haemodynamic response to exercise in relation to left atrial (LA) dynamics is unexplored. We sought to define whether abnormal LA dynamics during exercise may play a role in cardiac output (CO) limitation and tested its ability to predict outcome. A total of 195 HF patients with reduced (n = 105), mid-range (n = 48), and preserved (n = 42) left ventricular ejection fraction (LVEF) and 46 non-cardiac dyspnoea (NCD) subjects underwent cardiopulmonary imaging with assessment of LA strain and strain rate (sra). HF patients, irrespective of LVEF, exhibited a significantly impaired LA strain and LA sra at rest, during exercise and recovery compared to NCD subjects with a blunted response in CO and right ventricular to pulmonary circulation coupling. LA strain and LA sra during exertion were significantly correlated with peak stroke volume index, peak CO and peak cardiac power output (R = 0.33, 0.48, 0.50 and R = 0.36, 0.51, 0.52 for LA strain and LA sra, respectively; all P < 0.001). In HF, after adjustment for age, gender, left atrial volume index, peak mitral regurgitation > 2, peak LVEF and peak heart rate, a higher LA strain (1% increase) during exercise was associated with a higher peak stroke volume index (mL/m2 ), CO (L/min) and cardiac power output (mmHg L/min) at multivariable analyses (β-coefficients ± standard error = 0.23 ± 0.07, 0.046 ± 0.014 and 0.012 ± 0.004, respectively; P < 0.05). The same associations were found also for LA sra (absolute value) (1/s increase, β-coefficients ± standard error = 1.91 ± 0.68, 0.43 ± 0.14 and 0.12 ± 0.04, respectively; P < 0.05). Exercise LA strain (adjusted hazard ratio 0.94, 95% confidence interval 0.92-0.97, P < 0.001) and LA sra (adjusted hazard ratio 0.60, 95% confidence interval 0.43-0.84, P = 0.003) were associated with a worse outcome after adjusting for age and gender. In HF, LA dynamics may play a key role in exercise CO increase due to an impaired forward (left ventricular filling) and backward (right ventricular to pulmonary circulation uncoupling) combination of mechanisms, irrespective of LVEF. The blunted LA strain and LA sra reserve during exercise are associated with a worse cardiopulmonary performance and outcome.

P1743 The contribution of left atrial dysfunction to exercise intolerance in early heart failure with preserved left ventricular ejection fraction

Abstract Background Diagnosis of early heart failure with preserved ejection fraction (HFpEF) may be challenging because exertional dyspnea is not specific for heart failure, and biomarkers and indicators of volume overload may be absent at rest. We aimed to characterize the contribution of abnormal left atrial (LA) mechanical properties to exercise intolerance in early HFpEF (normal left ventricular filling pressures at rest but elevated during exercise). Methods Diastolic stress testing (DST) was performed in 104 patients with left ventricular ejection fraction ≥50%, in sinus rhythm, and no more than LV diastolic dysfunction grade I, referred for assessment of exertional dyspnoea. Patients exercised supine cycle ergometry at 60 rpm starting with a 3-min period of low-level 25-W workload followed by 25-W increments in 3-minute stages to maximum tolerated levels. According to DST, 43 patients were diagnosed with HFpEF (average mitral E-to-annular e′ ratio [E/e′] &amp;gt; 14, and peak TR velocity &amp;gt;2.8 m/sec at maximal exertion) and 61 as non-cardiac dyspnea (NCD). During the test, two-dimensional images, mitral E/e′, peak tricuspid regurgitation (TR) velociry, and two-dimensional LA mechanical parameters (longitudinal LA strain [LASR] and strain rate [LASRR] during reservoir phase and LA stiffness assessed as a ratio of mitral E/e′ ratio to LASR) were analysed at baseline, and at peak. Results HFpEF and NCD patients were similar in regard to the LA volume index (34.4 [30.2;39.4] vs. 33.6 [28.4;37.1] ml/m2), and NT-proBNP level (132 [80;238] vs. 129 [80;197] pg/ml). As compared with NCD patients, HFpEF patients displayed reduced LA reservoir function assessed by LASR (22.3 [18.9;25.6] vs. 24.2 [21.2;29.8] % at rest, and 25.3 [21.4;30.2] vs. 29.0 [24.2;33.3] % with exercise) and LASRR (0.78 [0.58;0.96] vs. 0.90 [0.68;1.12] /s at rest, and 1.10 [0.79;1.31] vs. 1.24 [1.03;1.56] s–1 with exercise) with increased LA stiffness (0.57 [0.44;0.70] vs. 0.42 [0.30;0.49] mmHg/% at rest, and 0.61 [0.46;0.74] vs. 0.40 [0.32;0.51] mmHg/% with exercise, all P &amp;lt; 0.05). Additionally, HFpEF patients showed smaller exercise elevation in LASRR (+31 [-5;77] vs. +47 [12;85] % as compared with resting values, P &amp;lt; 0.05). Exercised LA stiffness and reservoir strain correlated with exercise LV filling pressures estimated by mitral E/e′ ratio (r = 0.72 and r =–0.35, P &amp;lt; 0.001). LA stiffness showed a good diagnostic accuracy (area under the curve 0.75), and LA stiffness &amp;gt; 0.46 mmHg/% demonstrated reasonable sensitivity (79%) and specificity (71%) to diagnose HFpEF. Neither LV global longitudinal strain and ejection fraction at rest nor their exercise-induced elevation differed between HFpEF and NCD. Conclusion Impaired LA reservoir function and increased stiffness are associated with exercise intolerance in patients with early HFpEF, while LV systolic function seems preserved in this stage of the disease. LA stiffness provides HFpEF diagnostic potential in ambulatory patients with dyspnea

NTproBNP and BNP level in acute heart failure patients aged 75 or older are higher than in non-cardiac dyspnoea

To evaluate the level of N-terminal pro brain natriuretic peptide and brain natriuretic peptide (NTproBNP and BNP) for acute heart failure (AHF) diagnosis in patients aged 75 or older. In a previous smaller study of very old patients with acute dyspnoea, despite being independently associated with the cardiac aetiology, BNP level was higher in cardiac vs. respiratory origin of dyspnea. In total, 7822 patients aged 75 years or older, hospitalized in geriatrics, cardiologic and pneumologic department for acute dyspnoea in the enlarged Assistance Publique-Hôpitaux de Paris hospitals had a NTproBNP and a BNP measurement in the 48 hours after admission. Mean (SD) age was 85.5 (5.9) years, 55,5% ( n = 4190) of patients were women. 72% ( n = 5636) were admitted from the emergency department. 4800 (63,5%) patients had AHF diagnosis at discharge. The NTproBNP levels were significantly higher in the AHF group (median = 5598 ng/L, interquartile range = 2604;35000) than in the respiratory group (median = 1290 ng/L, interquartile range = 433;20200; P < 0.001). The BNP levels were significantly higher in the AHF group (median = 574 ng/L, interquartile range = 303;3140) than in the respiratory group (median = 152 ng/L, interquartile range = 66;813; P < 0.001) ( Fig. 1 ). In patients over 75 years of age consulting for acute dyspnea, NTproBNP and levels are higher in patients with AHF than in other cause of dyspnea. In this population, the threshold of natriuretic peptides for AHF diagnostic might be increased.

Amplified P-wave duration predicts new-onset atrial fibrillation in patients with heart failure with preserved ejection fraction.

Atrial fibrillation (AF) increases morbidity and mortality in heart failure with preserved ejection fraction (HFpEF), yet identification of HFpEF-patients at risk for new-onset AF is challenging. Amplified P-wave duration (APWD) non-invasively detects arrhythmogenic atrial substrate with high accuracy. We hypothesized that APWD may help in the prediction of new-onset AF in HFpEF. Patients with suspected HFpEF (n = 99, left ventricular ejection fraction > 50%, no evidence of valvulopathy, coronary artery disease, or non-cardiac dyspnea) underwent exercise testing with concomitant right-heart catheterization. Normal resting pulmonary capillary wedge pressure (PCWP; < 12mmHg) with an increase during exercise > 25.5mmHg/W/kg defined early HFpEF. Advanced HFpEF was diagnosed with PCWP > 12mmHg at rest. Arrhythmogenic atrial substrate (defined as APWD > 150ms) was investigated on digitized standard 12-lead ECGs and patients were followed for new-onset AF at 6-month intervals. Forty-seven patients had normal exercise haemodynamics and served as controls. Early and advanced HFpEF was diagnosed in 29 and 23 patients, respectively. Eighty-seven per cent of patients with advanced HFpEF had evidence of arrhythmogenic atrial substrate, (APWD 175 ± 29ms vs. 132 ± 14ms in controls, p < 0.0001), which was associated with a tenfold increased risk for new-onset AF during 4.6years of follow-up (hazard ratio [HR] 9.684, 95% CI 2.61-35.89, p < 0.0001). Early HFpEF was neither related to APWD (p = 0.395), nor to a higher risk for AF (HR 3.44, 95% CI 0.57-20.72, p = 0.178). Importantly, the presence of arrhythmogenic substrate was independent of left atrial indexed volume. The analysis of amplified P-wave duration (APWD) allows for the prediction of new-onset AF in patients with advanced HFpEF.

Echocardiographic subtypes of heart failure in consecutive hospitalised patients with dyspnoea

Heart failure with preserved ejection fraction (HFpEF) involves half of hospitalised patients with heart failure (HF), but estimates vary due to unclear diagnostic criteria. We performed a prospective observational study...

Impaired left atrial strain predicts abnormal exercise haemodynamics in heart failure with preserved ejection fraction.

Elevated left atrial (LA) pressure, particularly during exercise, is associated with symptomatic status and survival in patients with heart failure with preserved ejection fraction (HFpEF). We aimed to characterize the contribution of abnormal LA mechanical properties to exercise haemodynamics in HFpEF. Simultaneous echocardiography and right heart catheterization were performed in 71 subjects with left ventricular ejection fraction ≥ 50% referred for assessment of exertional dyspnoea. According to haemodynamic evaluation, 49 patients were diagnosed with HFpEF [pulmonary capillary wedge pressure (PCWP) ≥ 15 mmHg at rest and/or ≥ 25 mmHg at maximal exertion] and 22 as non-cardiac dyspnoea. Apical two- and four-chamber views were used for blinded two-dimensional LA speckle tracking analysis. HFpEF was characterized by impaired LA reservoir (24.3 ± 9.6 vs. 36.7 ± 8.4%, P < 0.001) and pump strain (-11.5 ± 3.2 vs. -17.0 ± 3.4%, P < 0.001); and increased stiffness (0.8 ± 0.7 vs. 0.2 ± 0.1 mmHg/%, P < 0.001). Reservoir and pump strain correlated with exercise PCWP (r = -0.64 and r = 0.72, P < 0.001), and remained independent predictors after adjusting for left ventricular mass index, LA volume index, mean E/e' and systolic blood pressure (B = -0.66 and B = 1.41, respectively, P < 0.001). LA stiffness was strongly related to B-type natriuretic peptide levels (r = 0.73, P < 0.001; B = 173.0, P < 0.001). Reservoir strain at cut-off of ≤ 33% predicted invasively verified HFpEF diagnosis with 88% sensitivity and 77% specificity, providing a net reclassification improvement of 12% in comparison to the 2016 European Society of Cardiology criteria for non-invasive diagnosis of HFpEF. Impaired LA reservoir and pump function and increased stiffness are associated with abnormal exercise haemodynamics in HFpEF. These markers provide significant HFpEF diagnostic utility in elderly ambulatory patients with dyspnoea.

Acute cardiac dyspnea in the emergency department: diagnostic value of N-terminal prohormone of brain natriuretic peptide and galectin-3.

ObjectiveThis study was performed to determine whether a dual-biomarker approach using N-terminal prohormone of brain natriuretic peptide (NT-proBNP) and galectin-3 optimizes the diagnosis and risk stratification of acute cardiac dyspnea. Atypical clinical manifestations and overlapping pathologies require objective and effective diagnostic methods to avoid treatment delays.MethodsThis prospective observational study included 208 patients who presented to the emergency department for acute dyspnea. NT-proBNP and galectin-3 were measured upon admission. The patients were divided into two groups according to the etiology of their clinical manifestations: cardiac and non-cardiac dyspnea. The patients’ New York Heart Association functional class, left ventricular ejection fraction, and discharge status were assessed.ResultsDiagnostic criteria for acute heart failure were fulfilled in 61.1% of the patients. NT-proBNP and galectin-3 were strongly and significantly correlated. Receiver operating characteristic analysis revealed similar areas under the curve for both markers in the entire group of patients as well as in the high-risk subsets of patients.ConclusionsThe diagnostic performance of NT-proBNP and galectin-3 is comparable for both the total population and high-risk subsets. Galectin-3 adds diagnostic value to the conventional NT-proBNP in patients with acute cardiac dyspnea, and its utility is of major interest in uncertain clinical situations.

A Simple, Evidence-Based Approach to Help Guide Diagnosis of Heart Failure With Preserved Ejection Fraction.

Diagnosis of heart failure with preserved ejection fraction (HFpEF) is challenging in euvolemic patients with dyspnea, and no evidence-based criteria are available. We sought to develop and then validate noninvasive diagnostic criteria that could be used to estimate the likelihood that HFpEF is present among patients with unexplained dyspnea to guide further testing. Consecutive patients with unexplained dyspnea referred for invasive hemodynamic exercise testing were retrospectively evaluated. Diagnosis of HFpEF (case) or noncardiac dyspnea (control) was ascertained by invasive hemodynamic exercise testing. Logistic regression was performed to evaluate the ability of clinical findings to discriminate cases from controls. A scoring system was developed and then validated in a separate test cohort. The derivation cohort included 414 consecutive patients (267 cases with HFpEF and 147 controls; HFpEF prevalence, 64%). The test cohort included 100 consecutive patients (61 with HFpEF; prevalence, 61%). Obesity, atrial fibrillation, age >60 years, treatment with ≥2 antihypertensives, echocardiographic E/e' ratio >9, and echocardiographic pulmonary artery systolic pressure >35 mm Hg were selected as the final set of predictive variables. A weighted score based on these 6 variables was used to create a composite score (H2FPEF score) ranging from 0 to 9. The odds of HFpEF doubled for each 1-unit score increase (odds ratio, 1.98; 95% CI, 1.74-2.30; P<0.0001), with an area under the curve of 0.841 ( P<0.0001). The H2FPEF score was superior to a currently used algorithm based on expert consensus (increase in area under the curve of 0.169; 95% CI, 0.120-0.217; P<0.0001). Performance in the independent test cohort was maintained (area under the curve, 0.886; P<0.0001). The H2FPEF score, which relies on simple clinical characteristics and echocardiography, enables discrimination of HFpEF from noncardiac causes of dyspnea and can assist in determination of the need for further diagnostic testing in the evaluation of patients with unexplained exertional dyspnea.

Natriuretic peptide B plasma concentration increases in the first 12 h of pulmonary edema recovery

BackgroundAccording to guidelines, single determination of B-type Natriuretic peptide (BNP) should be used for distinguishing between cardiac and non-cardiac acute dyspnea at the emergency room. BNP measurement is also recommended before hospital discharge in patients hospitalized for heart failure to assess prognosis and to evaluate treatment efficacy.In acute cardiogenic pulmonary edema, BNP is measured using a single BNP determination, but the temporal behavior of BNP during pulmonary edema recovery is unknown. MethodsFifty chronic low ejection fraction (<40%) heart failure patients (age 77 ± 9 years, 17 M-33F) admitted for acute pulmonary edema were studied. Patients were grouped according to 50% dyspnea recovery time into 3 groups: ≤30 min (n = 14), 30 to 60 min (n = 19), and > 60 min (n = 17). BNP was measured at arrival and 4, 8, 12 and 24 h afterwards. ResultsAt arrival, BNP was elevated in all patients without significant difference among groups. In the entire population, BNP median and interquartile range value were 791 (528–1327) pg/ml, 785(559–1299) pg/ml, 1014(761–1573) pg/ml, 1049(784–1412) pg/ml, 805(497–1271) pg/ml at arrival and 4, 8, 12 and 24 h afterwards, respectively, showing higher values at 8 and 12 h. This peculiar temporal behavior of BNP was shared by all study groups. Patients with the longest edema resolution showed the highest BNP level 8 and 12 h after admission. ConclusionsIn acute pulmonary edema, BNP increased up to 12 h after emergency admission regardless of dyspnea recovery time, making BNP quantitative meaning in the acute phase of pulmonary edema uncertain.

Assessment of left atrial size in addition to focused cardiopulmonary ultrasound improves diagnostic accuracy of acute heart failure in the Emergency Department.

Acute dyspnea is one of the main reasons for admission to Emergency Department (ED). Availability of ultraminiaturized pocket ultrasound devices (PUD) adds diagnostic power to the clinical examination. The aim of this study was to identify an integrated ultrasound approach for diagnosis of acute heart failure (acute HF), using PUD and combining evaluation from lung, heart and inferior vena cava (IVC). We included 102 patients presenting to the ED of "Antonio Cardarelli" Hospital in Naples (Italy) for acute dyspnea (AD). All patients underwent integrated ultrasound examination (IUE) of lung-heart-IVC, using PUD. The gold standard was the final diagnosis determined by two expert reviewers: acute heart failure (acute HF) or noncardiac dyspnea. We used 2×2 contingency tables to analyze sensitivity, specificity, positive and negative predictive value and accuracy of the three ultrasonic methods, and their combinations for the diagnosis of acute HF, comparing with the final, validated diagnosis. Lung ultrasound (LUS) alone exhibited a good sensitivity (100%) and specificity (82%) and had the highest accuracy (89%) among single modalities (heart and IVC) for the diagnosis of acute HF. The highest accuracy among all methods (96%) was obtained by the combination of positive LUS and either dilated left atrium or EF≤40% or both (all P<.01 vs single modalities). In patients presenting to ED, IUE using PUD is a useful extension of clinical examination and has a reliable diagnostic discriminant ability in the immediate evaluation of acute dyspnea. The combination of positive LUS with focused cardiac ultrasonography (FoCUS), including also dilated left atrium, substantially extends the spectrum of recognizable acute HF.

Acutely decompensated heart failure with preserved and reduced ejection fraction present with comparable haemodynamic congestion.

Congestion is a central feature of acute heart failure (HF) and its assessment is important for clinical decisions (e.g. tailoring decongestive treatments). It remains uncertain whether patients with acute HF with preserved ejection fraction (HFpEF) are comparably congested as in acute HF with reduced EF (HFrEF). This study assessed congestion, right ventricular (RV) and renal dysfunction in acute HFpEF, HFrEF and non-cardiac dyspnoea. We compared echocardiographic and circulating biomarkers of congestion in 146 patients from the MEDIA-DHF study: 101 with acute HF (38 HFpEF, 41 HFrEF, 22 HF with mid-range ejection fraction) and 45 with non-cardiac dyspnoea. Compared with non-cardiac dyspnoea, patients with acute HF had larger left and right atria, higher E/e', pulmonary artery systolic pressure and inferior vena cava (IVC) diameter at rest, and lower IVC variability (all P < 0.05). Mid-regional pro-atrial natriuretic peptide (MR-proANP) and soluble CD146 (sCD146), but not B-type natriuretic peptide (BNP), correlated with echocardiographic markers of venous congestion. Despite a lower BNP level, patients with HFpEF had similar evidence of venous congestion (enlarged IVC, left and right atria), RV dysfunction (tricuspid annular plane systolic excursion), elevated MR-proANP and sCD146, and renal impairment (estimated glomerular filtration rate; all P > 0.05) compared with HFrEF. In acute conditions, HFpEF and HFrEF presented in a comparable state of venous congestion, with similarly altered RV and kidney function, despite higher BNP in HFrEF.

Rapid assessment with physical examination in dyspnoeic cats: the RAPID CAT study.

To determine the underlying disease prevalence in acute feline dyspnoea and to examine whether historical and clinical examination findings can differentiate between acute cardiac and non-cardiac dyspnoea in cats in primary practice. We prospectively enrolled cats presenting with dyspnoea for the first time to primary practice between June 1, 2011 and October 31, 2016. We collected signalment, historical and clinical data at presentation using a standard form. Cases were investigated by primary clinicians, and the final diagnosis was confirmed by the authors. Records lacking critical data were excluded. Relationships between historical or clinical variables and dyspnoea aetiology were examined. Diagnostic test performance analyses were used to find optimal cut-off values for select historical or clinical variables that could differentiate cardiac and non-cardiac dyspnoea. Participants included 108 cats. A definitive diagnosis was reached in 92 cases; 60 were cardiac (65%), 15 respiratory (16%), 10 neoplastic (11%) and 7 traumatic (8%). Of cats with cardiac dyspnoea, 25% had a history of cough. A gallop sound, rectal temperature less than 37·5°C, heart rate of greater than 200 bpm and respiratory rate greater than 80 per minute were all useful to predict cardiac-associated dyspnoea. A triage algorithm using these findings in combination was designed to optimise the rapid diagnosis of probable cardiac dyspnoea. Dyspnoeic cats presenting in practice with hypothermia, tachycardia, gallop sounds or profound tachypnoea are likely to have a cardiac cause underlying their dyspnoea. Although diagnosis requires confirmation, clinicians may be able to stratify risk and prioritise further investigation based on these findings.

Natriuretic peptide hormones in congestive heart failure: challenges, clinical interpretation and review of studies

The primary action of natriuretic peptide hormones is to assist the heart in responding to the status of volume overload and subsequent stretching of the ventricles. Many studies have been done in the past decades that proved how useful is measuring brain natriuretic peptide (BNP) levels in diagnosing acute dyspnoea due to heart failure (HF) and to rule out non-cardiac dyspnoea. The major focus was on determining the optimal BNP level cutoffs that would help physicians in diagnosing acute cardiac dyspnoea early.The heart produces two natriuretic peptide hormones: atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). The most important stimulus in the secretion and release of these hormones, is stretch in the cardiac myocyte, which activates proBNP gene leading to de novo myocyte peptide synthesis and secretion. The more stretch that occurs, the higher level of these hormones which correlates with the severity of symptoms and prognosis. ProBNP originates from pre-proBNP, which is secreted by the ventricular musculature after volume or pressure overload. ProBNP is then further cleaved into two molecules, the biologically active BNP and the biologically inert NT-proBNP.In this manuscript, we will briefly review the pathophysiology of heart failure, BNP pathophysiology, clinical interpretation and limitation and review the most significant studies of BNP to determine the sensitivity and specificity of BNP in HF patients.

ST2 in Emergency Department Patients With Noncardiac Dyspnea

Serum levels of soluble ST2, a member of the interleukin-1 receptor family, predict mortality in emergency department (ED) patients with dyspnea secondary to acute heart failure and acute coronary syndrome. Elevated levels of ST2 have also been described in pulmonary disease, but it is unclear if these are associated with adverse outcomes. The hypothesis for this study was that elevated ST2 levels would be associated with 180-day mortality and 180-day return ED visits or hospital readmission in patients presenting to the ED with noncardiac causes of dyspnea. This prospective observational cohort study enrolled a convenience sample of patients presenting to a single academic tertiary care ED with a chief complaint of dyspnea. Exclusion criteria included dyspnea due to chest wall trauma, airway obstruction, and known cardiac etiology (new onset heart failure, prior heart failure with current brain natriuretic peptide > 500 pg/mL, presumed ischemic chest pain, elevated troponin, electrocardiogram changes indicating myocardial infarction or ischemia, heart transplant). ST2 levels were measured at ED presentation and compared between those with and without adverse outcomes. Staff were blinded to ST2 levels. Differences between groups were assessed using the Mann-Whitney U test. Of the 82 patients enrolled, 45 (55%) were female, 48 (59%) were African American, and 34 (42%) were hospitalized. The most frequent ED or hospital diagnosis was chronic obstructive pulmonary disease (COPD) or asthma, in 29 (35%) patients. At 180 days, 36 of 81 patients (44%) had return ED visits, 21 of 81 patients (26%) were readmitted, and five of 82 patients (6%) were deceased. Median ST2 level was 227 ng/mL in patients who died versus 32 ng/mL in those who survived (difference = 195 ng/mL, 95% confidence interval [CI] = 48 to 342 ng/mL, p = 0.006). Median ST2 level was 59 ng/mL in readmitted patients versus 31 ng/mL in nonreadmitted patients (difference = 28 ng/mL, 95% CI = -3 to 60 ng/mL, p = 0.036). Median ST2 levels were 41 ng/mL in patients with return ED visits versus 31 ng/mL in those without return visits (difference = 10 ng/mL, 95% CI = -10 to 20 ng/mL, p = 0.23). Patients with noncardiac dyspnea who died or required readmission to the hospital within 180 days had higher levels of ST2 compared with nonadmitted survivors. Further research into ST2 as a prognostic tool in pathologic processes not involving the heart, such as pulmonary disease, is warranted.

Biomarker Diagnostics in Acute Cardiac and Noncardiac Dyspnea: Is There a Role for Point-of-Care Testing?

The use of biomarkers in acute chest pain and dyspnea is well established and point-of-care testing (POCT) is increasingly used in emergency departments and chest pain units for this purpose. However, few data give evidence that POCT has advantages for the patient or the medical process over central laboratory testing. Especially for troponin testing in patients with myocardial infarction, the newest guidelines define prerequisites on diagnostic test quality which most POC assays do not fulfill. Additionally, no data are available showing that POCT has relevant effect on a change of physician’s diagnostic and therapeutic thinking compared to laboratory testing. Regarding patient outcomes and societal costs, central laboratory testing seems to be even superior to POCT. The main limit of currently available POC troponin assays is the higher limit of detection and higher imprecision compared to the new high sensitive laboratory assays. However, new upcoming POC technologies may perform comparable to today’s laboratory analyzers.

Differentiation of Cardiac and Noncardiac Dyspnea Using Bioelectrical Impedance Vector Analysis (BIVA)

BackgroundThere is no gold standard for the differential diagnosis of acute dyspnea despite the usefulness of N-terminal pro–B-type natriuretic peptide (NT-proBNP) and lung ultrasound. No study has evaluated the contribution of bioelectrical impedance vector analysis (BIVA) in discriminating between cardiac and noncardiac dyspnea. We sought to determine whether a relationship exists between ultrasound detection of lung congestion, NT-proBNP, and BIVA in patients with acute dyspnea. Methods and ResultsEligible patients were between 50 and 95 years, with an estimated glomerular filtration rate of ≥30 mL min−1 1.73 m−2, who presented to an emergency department with dyspnea. Dyspnea was classified by reviewers blinded to BIVA as cardiac or noncardiac based on physical examination, electrocardiogram, chest X-ray, NT-proBNP, and B-lines of lung congestion on ultrasound. Overall, 315 patients were enrolled (median age 77 years, 48% male). An adjudicated diagnosis of cardiac dyspnea was established in 169 (54%). Using BIVA, vector positions below −1 SD of the Z-score of reactance were associated with peripheral congestion (χ2 = 115; P < .001). BIVA measures were reasonably accurate in discriminating cardiac and noncardiac dyspnea (69% sensitivity, 79% specificity, 80% area under the receiver operating characteristic curve). ConclusionsIn patients presenting with acute dyspnea, the combination of BIVA and lung ultrasound may provide a rapid noninvasive method to determine the cause of dyspnea.

Exercise Hemodynamics Enhance Diagnosis of Early Heart Failure With Preserved Ejection Fraction

When advanced, heart failure with preserved ejection fraction (HFpEF) is readily apparent. However, diagnosis of earlier disease may be challenging because exertional dyspnea is not specific for heart failure, and biomarkers and hemodynamic indicators of volume overload may be absent at rest. Patients with exertional dyspnea and ejection fraction >50% were referred for hemodynamic catheterization. Those with no significant coronary disease, normal brain natriuretic peptide assay, and normal resting hemodynamics (mean pulmonary artery pressure <25 mm Hg and pulmonary capillary wedge pressure [PCWP] <15 mm Hg) (n=55) underwent exercise study. The exercise PCWP was used to classify patients as having HFpEF (PCWP ≥25 mm Hg) (n=32) or noncardiac dyspnea (PCWP <25 mm Hg) (n=23). At rest, patients with HFpEF had higher resting pulmonary artery pressure and PCWP, although all values fell within normal limits. Exercise-induced elevation in PCWP in HFpEF was confirmed by greater increases in left ventricular end-diastolic pressure and was associated with blunted increases in heart rate, systemic vasodilation, and cardiac output. Exercise-induced pulmonary hypertension was present in 88% of patients with HFpEF and was related principally to elevated PCWP, as pulmonary vascular resistances dropped similarly in both groups. Exercise PCWP and pulmonary artery systolic pressure were highly correlated. An exercise pulmonary artery systolic pressure ≥45 mm Hg identified HFpEF with 96% sensitivity and 95% specificity. Euvolemic patients with exertional dyspnea, normal brain natriuretic peptide, and normal cardiac filling pressures at rest may have markedly abnormal hemodynamic responses during exercise, suggesting that chronic symptoms are related to heart failure. Earlier and more accurate diagnosis using exercise hemodynamics may allow better targeting of interventions to treat and prevent HFpEF progression.