Prognostic role of right ventricular dilatation and troponin I elevation in acute pulmonary embolism

Acute pulmonary embolism continues to cause significant morbidity and mortality despite advances in diagnosis and treatment. This retrospective analysis aimed to determine whether the combination of elevated troponin I and right ventricular dilatation (RVD) could provide a more powerful predictor for risk evaluation. The study data comprised records of 110 patients with either high-probability ventilation/perfusion lung scan or positive spiral computed tomography. All cause 100-day mortality was 18.2%. The hypotension and RVD variables significantly influenced 100-day mortality. For the combination of RVD and raised troponin I, the 100-day mortality rate was 31%. Notably, the group with elevated troponin I and no RVD had a 100-day mortality rate of only 3.7%. The combination of RVD and elevated troponin had a positive predictive value of 31% and a negative predictive value of 88% for 100-day mortality. Compared with existing reports, conflicting conclusions for the individual prognostic role of elevated troponin I, cancer, and heart failure were obtained. These conflicting conclusions most likely resulted from inappropriate cut-off troponin I values and the modest sample size. In conclusion, the combination of elevated troponin and RVD was able to identify a subset of patients most likely to benefit from aggressive therapy.     

Prognostic significance of troponin elevation and right ventricular enlargement in acute pulmonary embolism

The troponin I values and echocardiographic data of 141 patients with acute pulmonary embolism (PE) were correlated with 30-day mortality. Patients with elevated troponin and right ventricular enlargement are at significantly greater risk for death after PE than patients with only 1 or with neither adverse prognostic marker.     

Regional right ventricular dysfunction in acute pulmonary embolism and right ventricular infarction.

BACKGROUND: A normally contracting right ventricular apex associated to a severe hypokinesia of the mid-free wall ('McConnell sign') has been considered a distinct echocardiographic pattern of acute pulmonary embolism. OBJECTIVE: To evaluate the clinical utility of the 'McConnell sign' in the bedside diagnostic work-up of patients presenting to the Emergency Department with an acute right ventricular dysfunction due to pulmonary embolism or right ventricular infarction. DESIGN: Among 201 patients, consecutively selected from our clinical database and diagnosed as having massive or submassive pulmonary embolism or right ventricular infarction, 161 were suitable for an echocardiographic review of regional right ventricular contraction and were included in the study. There were 107 cases with pulmonary embolism (group 1) and 54 cases with right ventricular infarction (group 2). All echocardiographic studies were randomly examined by two experienced and independent echocardiographers, blinded to the patient diagnosis and without Doppler informations. RESULTS: The McConnell sign was detected in 75 of 107 patients in group 1 (70%) and in 36 of 54 patients in group 2 (67%); the finding was absent in 32 cases in group 1 and in 18 cases in group 2 (P=0.657). The sensitivity, specificity, positive and negative predictive values of the McConnell sign for the diagnosis of pulmonary embolism were respectively 70, 33, 67 and 36%. CONCLUSIONS: In a clinical setting of patients with acute right ventricular dysfunction the McConnell sign cannot be considered a specific marker of pulmonary embolism.     

Cardiac cachexia is associated with right ventricular failure and liver dysfunction

Background

The mechanisms involved in cardiac cachexia remain poorly understood. We examined the association of right ventricular (RV) and hepatic dysfunction with cardiac cachexia.

Methods

We prospectively enrolled 118 patients with left ventricular ejection fraction (LVEF) ≤ 40%, which were subgrouped as follows: New York Heart Association (NYHA) class II (n = 59), NYHA class III without cachexia (n = 41) and NYHA class III with cachexia (n = 18). All patients underwent blood collection, echocardiography and exercise testing.

Results

Reduced systolic RV function (tricuspid annular plane systolic excursion [TAPSE] ≤ 15 mm), was present in 80% of cachectic patients. When comparing NYHA class II patients vs. non-cachectic and cachectic NYHA class III patients we found a stepwise decrease in systolic RV function (TAPSE 19 [16–23] vs. 16 [13–19] vs. 14 [9–15] mm, respectively; p < 0.001) and an increase in right atrial pressure (RAP; > 10 mm Hg: 6.8 vs. 27.5 vs. 75.0%, respectively; p < 0.001), indicating a higher degree of congestive right HF in cardiac cachexia. Systolic and diastolic function of the left ventricle did not differ between non-cachectic and cachectic patients in NYHA class III. Serum alkaline phosphatase and direct bilirubin correlated with TAPSE and RAP, and were highest in cachectic patients (all p ≤ 0.002), suggesting cholestatic dysfunction due to liver congestion. In multivariable regression analysis, RV dysfunction, cholestatic liver parameters and albumin were independently associated with the presence of cardiac cachexia.

Conclusion

Patients with cardiac cachexia display a more pronounced degree of right HF, cholestatic liver dysfunction and hypoalbuminemia compared to non-cachectic patients of similar LVEF and NYHA class.     

Cardiac inflammation contributes to right ventricular dysfunction following experimental pulmonary embolism in rats

Acute right ventricular (RV) failure following pulmonary embolism (PE) is a strong predictor of poor clinical outcome. Present studies test for an association between RV failure from experimental PE, inflammation, and upregulated chemokine expression. Additional experiments test if neutrophil influx contributes to RV dysfunction. PE was induced in male rats by infusing 24 microm microspheres (right jugular vein) producing mild hypertension (1.3 million beads/100 g, PE1.3), or moderately severe hypertension (2.0 million beads/100 g, PE2.0). Additional rats served as vehicle sham (0.01% Tween 20, Veh). In vivo RV peak systolic pressures (RVPSP) increased significantly, and then declined following PE2.0 (51 +/- 1 mm Hg 2 h; 49 +/- 1, 6 h; 44 +/- 1, 18 h). RV generated pressure of isolated, perfused hearts was significantly reduced in PE2.0 compared with PE1.3 or Veh. MCP-1 protein (ELISA) was elevated 21-fold and myeloperoxidase activity 95-fold in RV of PE2.0 compared with Veh or PE1.3. CINC-1, CINC-2, MIP-2, MCP-1, and MIP-1alpha mRNA also increased in RV of PE2.0. Histological analysis revealed massive accumulation of neutrophils (selective esterase stain) and monocyte/macrophages (CD68, ED-1) in RV of PE2.0 hearts in regions of myocyte damage. Electron microscopy showed myocyte necrosis and phagocytosis by inflammatory cells. LV function was normal and did not show increased inflammation after PE2.0. Treatment with anti-PMN antibody reduced RV MPO activity and prevented RV dysfunction. Conclusions-PE with moderately severe pulmonary hypertension (PE2.0) resulted in selective RV dysfunction, which was associated with increased chemokine expression, and infiltration of both neutrophils and monocyte/macrophages, indicating that a robust immune response occurred with RV damage following experimental PE. Experimental agranulocytosis reduced RV, suggesting that neutrophil influx contributed to RV damage.     

Role of electrocardiography in identifying right ventricular dysfunction in acute pulmonary embolism

The role of electrocardiography in identifying right ventricular (RV) dysfunction in acute pulmonary embolism (APE) was evaluated in 81 patients with APE. The electrocardiographic markers studied were T-wave inversion in leads V1 to V3, the S1Q3T3 pattern, right bundle branch block, and sinus tachycardia. T-wave inversion in leads V1 to V3 had the greatest sensitivity and diagnostic accuracy for identifying RV dysfunction in patients with APE. The S1Q3T3 pattern and right bundle branch block had good specificity but moderate accuracy.     

急性肺栓塞并右心室功能不全心电图表现及临床应用

目的探讨急性肺栓塞(Acute Pulmonary Embolism APE)合并右心功能不全(Right Ventricular Dysfunction RVD)时心电图(ECG)的表现及临床应用价值。方法根据超声心动图(TTE)是否存在RVD,将105名APE患者分为:A组合并RVD 47例;B组无RVD 58例。分析比较两组患者的心电图表现及临床预后。结果 (1)心电图表现比较:T波倒置,V1-V3导联、V1及a VR导联ST段抬高,完全性右束支阻滞(complete right branch block CRBBB),SIQIIITIII,A组高于B组;(2)超声心动图指标:三尖瓣返流速度,肺动脉收缩压A组更高;(3)D-二聚体,达到临床终点的人数、中心肺动脉栓塞发生率A组更高。结论 APE合并RVD的患者临床预后差,更容易出现T波倒置,CRBBB,右胸及a VR导联ST段抬高,SIQIIITIII等一系列心电图表现。     

急性肺栓塞患者右室功能不全与肺血流灌注的相关性

目的观察血压正常的急性肺栓塞患者右室超声心动指标与肺血管阻塞严重程度相关性及治疗有效性的预测价值。方法回顾我院6年间收治的56例血压正常的急性肺栓塞患者的临床资料,分析其超声心动图所测得的右室收缩末期及舒张末期面积与肺灌注扫描灌注缺损数和增强螺旋CT所代表的肺血管阻塞之间的相关性。结果与正常对照相比,肺栓塞患者右室舒张末面积和收缩末面积增大,且与肺灌注缺损数呈正相关（r=0.76,P<0.01;r=0.77,P<0.01）,而舒张与收缩末面积的变化率则降低,与肺灌注缺损数呈负相关（r=-0.44,P<0.01）。增强CT显示血管阻塞越广泛,收缩末面积越大（P<0.05）,舒张与收缩末面积的变化率越小（P<0.05）。治疗有效时,肺灌注缺损数随右室功能的好转而降低。结论血压稳定的急性肺栓塞患者右室功能的异常程度与肺血管的阻塞程度密切相关,右室功能的检查可用于观察肺灌注情况以及治疗有效情况的相关指标。     

Association of right ventricular dysfunction with in-hospital mortality in patients with acute pulmonary embolism and reduction in mortality in patients with right ventricular dysfunction by pulmonary embolectomy

Twenty-one of 64 patients (33%) with pulmonary embolisms with right ventricular (RV) dilation and 6 of 126 patients (5%) with pulmonary embolisms without RV dilation died during hospitalization (p <0.001). In the 64 patients with RV dilation, in-hospital mortality occurred in 2 of 18 hemodynamically unstable patients (11%) who underwent pulmonary embolectomy, in 2 of 6 hemodynamically stable patients (33%) treated with thrombolytic therapy plus intravenous heparin, and in 17 of 40 hemodynamically stable patients (43%) treated with intravenous heparin (p <0.025 comparing pulmonary embolectomy with no pulmonary embolectomy).     

Diagnosis of right ventricular dysfunction in acute pulmonary embolism using helical computed tomography

Forty-six consecutive patients with pulmonary embolism (PE) who underwent pulmonary angiography, helical computed tomography (CT), and echocardiography in the investigators' emergency department were studied. It was determined that the CT right ventricular (RV)/left ventricular (LV) end-diastolic area ratio was correlated with PE obstruction and echocardiography. A CT RV/LV area ratio >1 had a sensitivity of 88% and a specificity of 88% in diagnosing significant PE. The present study suggests that helical CT may be used as a triage tool in acute PE for selecting high-risk patients, using calculation of the RV/LV area ratio to detect RV dysfunction.     

Massive pulmonary embolism associated with a right ventricular myxoma

A 12 year old boy had a massive pulmonary embolism associated with a right ventricular myxoma. This caused complete occlusion of the main trunk of the left pulmonary artery and of a branch of the right pulmonary artery supplying the basal area of the lower lobe of the right lung. The patient died despite two surgical attempts to remove the tumor clots. To our knowledge this constitutes the first report of a massive pulmonary artery embolism associated with a right ventricular myxoma.     

Cardiac troponin I release in acute pulmonary embolism in relation to the duration of symptoms

PURPOSE: To evaluate the release of cardiac troponin I in normotensive patients with acute pulmonary embolism in relation to the duration of symptoms. METHODS: Fifty-seven normotensive patients with acute pulmonary embolism were included in the study. Patients were divided into two groups based on the duration of symptoms at presentation: symptoms of < or =72 h, group A; symptoms of >72 h, group B. Serum cardiac troponin I levels were measured at presentation. RESULTS: Mean age was 63+/-18 years and 23 (40%) patients were males. Thirty-three (58%) patients had symptoms of < or =72 h (group A) and 24 (42%) had symptoms of >72 h (group B). Both groups had similar prevalence of right ventricular dysfunction on echocardiography (55% [n=18] in group A vs. 42% [n=10] in group B, p=NS). Sixteen patients had elevated serum cardiac troponin I (mean+/-S.D. 3.3+/-2.3 ng/ml, range 0.6-8.3 ng/ml). Elevated serum cardiac troponin I was strongly associated with right ventricular dysfunction (p=0.015). All patients with elevated serum cardiac troponin I (n=16) were in group A (p<0.0001). Twelve of 18 (67%) patients with (p=0.0005) and 4 of 15 (27%) patients without (p=NS) right ventricular dysfunction had elevated serum cardiac troponin I. Thirteen of 16 (81%) patients with elevated serum cardiac troponin I had duration of symptoms < or =24 h at presentation. CONCLUSIONS: The dynamics of cardiac troponin I release in acute pulmonary embolism in patients who present with symptoms of < or =72 h duration could be different from those who present with longer duration of symptoms. Therefore, the use of cardiac troponin I in risk stratification of acute pulmonary embolism might be limited to the patients presenting within 72 h of the onset of symptoms.     

The spatial ventricular gradient is associated with adverse outcomes in acute pulmonary embolism

Background

The spatial ventricular gradient (SVG) is a vectorcardiographic measurement that reflects cardiac loading conditions via electromechanical coupling.

Objectives

We hypothesized that the SVG is correlated with right ventricular (RV) strain and is prognostic of adverse events in patients with acute pulmonary embolism (PE).

Methods

Retrospective, single-center study of patients with acute PE. Electrocardiogram (ECG), imaging, and outcome data were obtained. SVG components were regressed on tricuspid annular plane systolic excursion (TAPSE), qualitative RV dysfunction, and RV/left ventricular (LV) ratio. Odds of adverse outcomes (30-day mortality, vasopressor requirement, or advanced therapy) after PE were regressed on demographics, RV/LV ratios, traditional ECG signs of RV dysfunction, and SVG components using a logit model.

Results

ECGs from 317 patients (48% male, age 63.1 ± 16.6 years) with acute PE were analyzed; 36 patients (11.4%) experienced an adverse event. Worse RV hypokinesis, larger RV/LV ratio, and smaller TAPSE were associated with smaller SVG X and Y components, larger SVG Z components, and smaller SVG vector magnitude (p < .001 for all). In multivariable logistic regression, odds of adverse events after PE decreased with increasing SVG magnitude and TAPSE (OR 0.32 and 0.54 per standard deviation increase; p = .03 and p = .004, respectively). Receiver operating characteristic (ROC) analysis showed that, when combined with imaging, replacing traditional ECG criteria with the SVG significantly improved the area under the ROC from 0.70 to 0.77 (p = .01).

Conclusion

The SVG is correlated with RV dysfunction and adverse outcomes in acute PE and has a better prognostic value than traditional ECG markers.     

Usefulness of combined assessment with computed tomographic signs of right ventricular dysfunction and cardiac troponin T for risk stratification of acute pulmonary embolism

The aim of this study was to evaluate the incremental value of combined assessment with computed tomographic (CT) signs of right ventricular (RV) dysfunction and cardiac troponin T level for predicting early death or adverse outcomes due to acute pulmonary embolism (PE). One hundred seventy-three non-high-risk patients with acute PE, confirmed by CT pulmonary angiography, were retrospectively evaluated. The area under the curve and hazard ratio of CT signs and troponin T levels were compared for predicting early death or adverse outcomes. Patients were classified into intermediate- and low-risk groups on the basis of CT signs and troponin T levels, and mortality was compared. Seventeen patients (9.8%) died within 3 months. Early mortality of intermediate-risk patients (14% to 19%) was higher than that of low-risk patents (2% to 6%). A ratio of RV volume to left ventricular volume > 1.5 had the highest area under the curve (0.709) and hazard ratio (5.402) for predicting early death. The combination of CT signs and elevated troponin T level had an increased area under the curve and hazard ratio for predicting early death and adverse outcomes compared to those of CT signs or elevated troponin T level alone. In conclusion, the combined assessment of the ratio of RV volume to left ventricular volume and an elevated troponin T level provided incrementally more prognostic information in non-high-risk patients with acute PE compared to the single predictor of CT signs or troponin T level.     

Regional right ventricular strain pattern in patients with acute pulmonary embolism

Aims: Right ventricular (RV) dysfunction is a frequent consequence of pulmonary embolism (PE) and a marker of increased risk. However, current qualitative methods assessing RV function are imprecise. We sought to determine whether RV strain analysis would have clinical utility in patients with PE compared with normal controls. Methods and results: We compared 75 acute PE subjects (mean age 54 ± 16) with 30 normal controls (mean age 50 ± 15). Regional RV longitudinal strain was assessed using offline speckle tracking software to obtain strain and strain rate data from the basal, mid, and apical free wall and septum. Global RV free wall and septal strain was significantly reduced in PE subjects (?14.17 (±5.96) vs ?24.92 (±4.16), P < 0.0001; ?14.99 (±5.55) vs ?18.54 (±7.34), P = 0.0082). Regional RV strain was markedly reduced in PE subjects in all regions of the free wall and in the mid and basal septum (P < 0.05). Strain rates of PE subjects were significantly reduced in all segments of the RV free wall (P < 0.05). In 36 PE subjects with regional RV dysfunction (“McConnell sign”), strain in the apical free wall was significantly reduced in comparison to those without (?10.08 vs ?13.51; P = 0.0420), in parallel with higher RV:LV ratios (1.30, ±1.01 vs 0.78, ±0.16; P = 0.0035) and lower RV fractional area change (32.06, ±14.42 vs 42.52, ±11.61; P = 0.0021). Conclusions: Regional RV longitudinal strain is altered in the free wall and mid and basal septum in subjects with acute PE. Strain rates are only reduced in the RV free wall. (Echocardiography 2012;29:464‐470)     

Cardiac troponin I elevation in hospitalized patients without acute coronary syndromes

Increase of cardiac troponins occurs in a variety of clinical situations in the absence of an acute coronary syndrome (ACS). Few data exist regarding the incidence, clinical characteristics, and predictive value of various cardiac diagnostic tests and outcome of patients with a non-ACS-related troponin increase. We studied 883 consecutive hospitalized patients with increased cardiac troponin I levels. The discharge diagnosis was reclassified and troponin increase attributed to ACS or another process. Clinical data and results of cardiac diagnostic tests were collected. Patients were followed for a median of 30 months. Three hundred eleven patients were classified as having a non-ACS-related troponin increase (35.2%). An alternative explanation for troponin increase was found in 99% of these patients. Troponin level had poor accuracy in discriminating patients with and without ACS (area under the receiver operating characteristics curve 0.63). Coronary angiography was frequently unhelpful in excluding a non-ACS-related troponin increase because 77% of patients in the non-ACS group had significant flow-limiting coronary artery disease. Patients with non-ACS-related troponin increase had significantly higher in-hospital (hazard ratio 2.8, 95% confidence interval 2.0 to 3.8) and long-term (hazard ratio 2.0, 95% confidence interval 1.6 to 2.5) mortalities compared with patients with ACS. In conclusion, cardiac troponin level is frequently increased in hospitalized patients in the absence of an ACS and portends poor short- and long-term outcomes. Most of these patients have an alternative explanation for cardiac troponin increase. Cardiac diagnostic procedures are frequently unhelpful in excluding a non-ACS-related troponin increase.