A Case of Amitriptyline-induced Myocarditis.

Amitriptyline is a widely prescribed tricyclic antidepressant (TCA) with a very concerning cardiotoxicity profile, but it is one that has not been discussed much in literature. Here, we present a case of amitriptyline toxicity presenting as myocarditis with pericardial involvement. A 21-year-old male with no previous cardiac history presented to the emergency department (ED) with a decreased level of consciousness after an amitriptyline overdose as a suicidal attempt. For concerns with airway protection, the patient was intubated and subsequently admitted to the intensive care unit (ICU). An electrocardiogram (EKG) showed sinus tachycardia, prolonged QRS complex, prolonged QTc interval, and nonspecific ST-T wave changes. Intravenous fluid resuscitation and sodium bicarbonate were administered with a target blood pH of 7.5 to 7.55. Two days later, the patient was taken off mechanical ventilation and improved clinically. However, troponin levels began to rise with a peak level of 4.08 µg/L. He then began having fevers, elevated white blood cell counts (WBCs), and elevated inflammatory markers. Transthoracic echo (TTE) revealed an ejection fraction (EF) of 45%-50%, no wall segment motion abnormalities, and a mild-to-moderate pericardial effusion. Cardiac magnetic resonance (CMR) was done, which revealed changes indicative of acute myocarditis, moderate pericardial effusion, a calculated EF of 45% with a moderate left ventricular dilation, and no coronary artery stenosis or anomalous coronary artery origin. Given the patient's age, the absence of cardiac risk factors, and the presence of an amitriptyline overdose along with his EKG, TTE, and CMR findings, we hypothesize that this myocarditis with pericardial involvement is due to amitriptyline-induced direct toxicity.

Influence of Left Ventricular Hypertrophy on In-Hospital Outcomes in Acute Exacerbation of Chronic Obstructive Pulmonary Disease.

Left ventricular hypertrophy (LVH) is associated with worse outcomes in chronic obstructive pulmonary disease (COPD); however, its role in an acute exacerbation of COPD (AECOPD) has not been reported. This was a retrospective cohort study during 2008-2012 at an academic medical center. AECOPD patients >18 years with available echocardiographic data were included. LVH was defined as LV mass index (LVMI) >95 g/m2 (women) and >115g/m2 (men). Relative wall thickness was used to classify LVH as concentric (>0.42) or eccentric (<0.42). Outcomes included need for and duration of non-invasive ventilation (NIV) and mechanical ventilation (MV), NIV failure, intensive care unit (ICU) and total length of stay (LOS), and in-hospital mortality. Two-tailed p < 0.05 was considered statistically significant. Of 802 patients with AECOPD, 615 patients with 264 (42.9%) having LVH were included. The LVH cohort had higher LVMI (141.1 ± 39.4 g/m2 vs. 79.7 ± 19.1 g/m2; p < 0.001) and lower LV ejection fraction (44.5±21.9% vs. 50.0±21.6%; p ≤ 0.001). The LVH cohort had statistically non-significant longer ICU LOS, and higher NIV and MV use and duration. Of the 264 LVH patients, concentric LVH (198; 75.0%) was predictive of greater NIV use [82 (41.4%) vs. 16 (24.2%), p = 0.01] and duration (1.0 ± 1.9 vs. 0.6 ± 1.4 days, p = 0.01) compared to eccentric LVH. Concentric LVH remained independently associated with NIV use and duration. In-hospital outcomes in patients with AECOPD were comparable in patients with and without LVH. Patients with concentric LVH had higher NIV need and duration in comparison to eccentric LVH.

A patient selection score for cardiac resynchronization therapy.

BACKGROUND: We hypothesized a patient selection score (PSS) may improve patient selection for cardiac resynchronization therapy (CRT). METHODS: Of 136 patients who received CRT, group A included 100 study patients and group B 36 patients for validation. A positive response to CRT was a left ventricular (LV) end-systolic volume decrease of ≥15% and survival from heart failure at end of follow-up. RESULTS: Of 100 group A patients, 37 (37%) were CRT responders during 14-month follow-up. A 7-point PSS was generated based on six variables. The cutoff point for PSS to predict a positive response to CRT was >4 by receiver operating characteristic (ROC) analysis. The area under the ROC curve (AUC) for PSS to predict CRT response was 0.94 (P = 0.0001). CRT responders in patients with a PSS > 4 and ≤4 were 33/40 (83%), and 4/60 (7%), respectively (P < 0.001). Multivariate Cox proportional regression analysis showed that PSS was related to CRT response (hazard ratio = 10.3, P < 0.0001). The CRT response rate in patients with a PSS > 4 in Group B was also significantly higher compared to a PSS ≤ 4 (88% vs. 16%, P < 0.001). The AUC for PSS to predict a CRT response in Group B was 0.91 (P = 0.0001). CONCLUSIONS: Patients with a PSS >4 are the most likely to respond to CRT. Using this score system, a PSS score >4 can predict the probability of a CRT response up to 88% in patients with heart failure and a wide QRS duration.

Impact of left atrial volume in prediction of outcome after cardiac resynchronization therapy.

UNLABELLED: Left atrial volume index (LAVI) as a predictor of mortality has not been well investigated in patients with cardiac resynchronization therapy (CRT). The purpose of this study is to evaluate the impact of LAVI in predicting mortality in CRT patients. METHODS: We studied 100 consecutive patients who received CRT (male 73, age 69.9 ± 9.6 years). The follow-up duration of all echocardiographic measurements was 14.4 ± 10.5 months after CRT. LAVI was measured from apical views on two-dimensional echocardiography by bi-plane rule. A decrease of left ventricular end systolic volume ≥ 15% after CRT was defined as a positive response to CRT. RESULTS: The mean LAVI at baseline was 59.9 ± 22.7 ml/m(2). LAVI in patients who died (78.2 ± 27.5 ml/m(2)) was significantly greater than those who survived (55.9 ± 19.5 ml/m(2), p<0.0001) during follow-up of 17 ± 10.6 months. The area under ROC curve (AUC) for LAVI predicting death was 0.77 (p=0.0001). The cutoff point for LAVI predicting death was LAVI>59.4 ml/m(2). LAVI>59.4 ml/m(2) was related to mortality by Cox proportional univariate regression [hazard ratio (HR)=5.15, 95% CI=1.48-17.93, p=0.01]. After adjustment for the variables with significant difference by univariate regression, LAVI>59.4 ml/m(2) was continuously related to mortality by multivariate regression (HR=4.56, 95% CI, 1.30-15.97, p=0.02). LAVI>59.4 ml/m(2) was associated with a near 5-fold increase in mortality during follow-up of 17 ± 10.6 months. CONCLUSION: Patients who have LAVI>59.4 ml/m(2) continue to have increased mortality despite CRT.

Thoracic aortic atheroma severity predicts high-risk coronary anatomy in patients undergoing transesophageal echocardiography.

INTRODUCTION: We hypothesized a relationship between severity of thoracic aortic atheroma (AA) and prevalence of high-risk coronary anatomy (HRCA). MATERIAL AND METHODS: We investigated AA diagnosed by transesophageal echocardiography and HRCA diagnosed by coronary angiography in 187 patients. HRCA was defined as ≥ 50% stenosis of the left main coronary artery or significant 3-vessel coronary artery disease (≥ 70% narrowing). RESULTS: HRCA was present in 45 of 187 patients (24%). AA severity was grade I in 55 patients (29%), grade II in 71 patients (38%), grade III in 52 patients (28%), grade IV in 5 patients (3%), and grade V in 4 patients (2%). The area under receiver operating characteristic curve for AA grade predicting HRCA was 0.83 (p = 0.0001). The cut-off points of AA to predict HRCA was > II grade. The sensitivity and specificity of AA > grade II to predict HRCA were 76% and 81%, respectively. After adjustment for 10 variables with significant differences by univariate regression, AA > grade II was related to HRCA by multivariate regression (odds ratio = 7.5, p< 0.0001). During 41-month follow-up, 15 of 61 patients (25%) with AA >grade II and 10 of 126 patients (8%) with AA grade ≤ 2 died (p= 0.004). Survival by Kaplan-Meier plot in patients with AA > grade II was significantly decreased compared to patients with AA ≤ grade II (p= 0.002). CONCLUSIONS: AA > grade II is associated with a 7.5 times increase in HRCA and with a significant reduction in all-cause mortality.

Electrocardiographic abnormalities of takotsubo cardiomyopathy in a patient with paced ventricular rhythm.

Takotsubo cardiomyopathy (TCM) is a unique cardiomyopathy characterized by chest pain, ECG, and regional wall motion abnormalities closely mimicking acute myocardial infarction, in the absence of significant coronary artery disease. Classic ECG changes of TCM include ST elevation or T wave inversion. However, ECG abnormalities of TCM in patients with paced ventricular rhythms have not been well characterized. Herein, we report the case of an 85-year-old pacemaker dependant female who was diagnosed with TCM four weeks following the demise of her husband. Abnormal negative T wave concordance in precordial leads and QT interval prolongation were the only new ECG findings and these reverted back to baseline on followup.

Evaluation of left ventricular dyssynchrony using combined pulsed wave and tissue Doppler imaging.

INTRODUCTION: The combination of pulsed wave (PW) and tissue Doppler imaging (TDI) has been proposed as a new method to assess left ventricular (LV) mechanical dyssynchrony (LVMD), but results have not been validated. We investigated the correlation of a combination of PW and TDI with a positive response to cardiac resynchronization therapy (CRT). MATERIAL AND METHODS: We studied 108 consecutive patients who received CRT. Patients with atrial fibrillation were excluded. The time difference (T(PW-TDI)) between onset of QRS to the end of LV ejection by PW (T(PW)) and onset of QRS to the end of the systolic wave in LV basal segments with greatest delay by TDI (T(TDI)) was measured before CRT and during short-term and long-term follow-up. RESULTS: The T(PW-TDI) interval before CRT was 74 ±48 ms. Intra-observer variabilities for T(PW) and T(TDI) were 1.5 ±0.24% and 1 ±0.17%. Inter-observer variabilities for T(PW) and T(TDI) were 1 ±0.36% and 1 ±0.64%, respectively. T(PW-TDI) > 50 ms was defined as the cutoff value for diagnosis of LVMD by receiver operating curve (ROC) analysis. During follow-up of 15 ±11 months, the sensitivity and specificity of TP(PW-TDI) to predict a positive response to CRT were 98% and 82%, respectively. The area under the ROC curve was 0.92. There was a significant agreement between LVMD determined by T(PW-TDI) and the positive response to CRT (κ=0.80). CONCLUSIONS: Left vertricular dyssynchrony detected by the method combining PW and TDI demonstrated a high reproducibility, sensitivity, specificity and agreement with a positive response to CRT.

Effect of medical therapy on left ventricular ejection fraction in patients with systolic heart failure and narrow QRS duration with and without ischemic heart disease and left ventricular mechanical dyssynchrony.

We studied 99 consecutive patients with class III-IV systolic heart failure with a left ventricular ejection fraction (LVEF) < or =35% and a QRS duration <120 milliseconds. Patients with cardiac resynchronization therapy were excluded. Echocardiography was performed in all patients before and after optimal standard heart failure therapy. The septal-to-posterior wall motion delay (SPWMD) > or =130 milliseconds on echocardiogram was defined as left ventricular mechanical dyssynchrony (LVMD). Sixty-nine of 99 patients (70%) had ischemic heart disease. During follow-up of 15.2 +/- 9.8 months, LVEF improvement > or =15% was greater patients in nonischemic group (50%, 15/30) than in ischemic group (9%, 6/69; P < 0.001). After adjustment for age, gender, and clinical and echocardiographic characteristics, ischemic heart disease and grade of coronary disease were persistently related to LVEF improvement > or =15% (P = 0.03 and 0.02, respectively). Twenty of 99 patients (20%) had SPWMD > or =130 milliseconds (LVMD group), and 79 of 99 patients (80%) had SPWMD <130 milliseconds (non-LVMD group). LVEF increased in both groups (P = 0.005) during follow-up, but the percentage of patients with LVEF improvement > or =15% in LVMD was greater compared with patients without LVMD (40% versus 16%, respectively, P = 0.03). In conclusion, the improvement of LVEF in patients with systolic heart failure and narrow QRS was greater in patients with nonischemic heart disease and LVMD compared with patients with ischemic heart disease and absence of LVMD during medical therapy without cardiac resynchronization therapy.

Thromboembolism in patients with atrial fibrillation with and without left atrial thrombus documented by transesophageal echocardiography.

The incidence of cerebrovascular events (CVEs) was investigated in 95 consecutive patients with atrial fibrillation (AF) with left atrial thrombus (LAT) diagnosed by transesophageal echocardiography (TEE) and in 131 age- and sex-matched AF patients without LAT. Compared with patients without LAT, patients with LAT had a larger left atrial diameter (49 versus 44 mm, P < 0.0001), a lower left ventricular ejection fraction (40% versus 50%, P < 0.0001), a higher prevalence of spontaneous echocardiographic contrast (88% versus 25%, P < 0.001), a reduced left atrial appendage emptying velocity (0.25 versus 0.41 cm/s, P < 0.0001), and less use of antiarrhythmic drugs (61% versus 76%, P = 0.03). Before TEE, the prevalence of prior CVE was higher in LAT patients (20%) compared with patients without LAT (8%) (P = 0.01). Fifty-four of 95 LAT patients (57%) and 81 of 131 non-LAT patients (62%) were on warfarin before TEE. The incidence of prior CVE in LAT patients without warfarin (32%) was higher than that in non-LAT patients without warfarin (10%) (P = 0.02). The mortality rate in LAT patients with an international normalized ratio (INR) >or= 2.0 (42%) was higher than that in patients without LAT and an INR >or= 2.0 (11%) (P < 0.001). Fifty-one of 95 LAT patients (54%) underwent repeat TEE before cardioversion (48 patients received warfarin therapy). The thrombus resolved in 40 of 51 patients (78%) after the first TEE. There was no significant difference in INR between the patients with persistent and resolved LAT. AF patients with persistent LAT had a higher incidence of CVE (45%) than the patients with resolved LAT (5%) (P = 0.003). We suggest that patients with LAT be treated with warfarin to maintain an INR between 2.5 and 3.5 rather than between 2.0 and 3.0 because they are at a high risk for new thromboembolism.

Cardiac resynchronization therapy in patients with intrinsic and right ventricular pacing-induced left bundle branch block pattern.

We studied 95 consecutive patients, mean age 70 years, who received cardiac resynchronization therapy (CRT) for class III or IV heart failure with a left ventricular (LV) ejection fraction < or =35% and a QRS duration > or =120 ms. Sixty-seven patients had intrinsic left bundle branch block (LBBB) (group 1), and 28 patients had right ventricular pacing-induced LBBB (group 2). The time difference (TPW-TDI) between onset of QRS to the end of LV ejection by pulsed wave Doppler and onset of QRS to the end of systolic wave in the basal segment with greatest delay by tissue Doppler imaging was measured before CRT and at the last follow-up after CRT. TPW-TDI >50 ms was defined as left ventricular mechanical dyssynchrony. A positive response to CRT was defined as LV volume at end-systole decreasing > or =15% after CRT. The percentage of CRT responders in group 2 was significantly greater than that in group 1 (68% versus 42%, P = 0.04) during follow-up of 16 months. After adjusting for age, gender, and clinical features, this pattern of CRT response persisted (P = 0.008). Similarly, there was a greater reduction in QRS duration in group 2 (178 ms) after CRT versus 154 ms for group 1, P = 0.01. There was no significant difference in TPW-TDI between the 2 groups at baseline or at follow-up. There was no significant difference in mortality (15% versus 14%) and Kaplan-Meier survival plot during follow-up. Patients with heart failure and right ventricular pacing-induced LBBB have a better response rate to CRT than patients with intrinsic LBBB. The change in left ventricular mechanical dyssynchrony after CRT was similar in these 2 groups of patients.

Effect of mitral regurgitation on cerebrovascular accidents in patients with atrial fibrillation and left atrial thrombus.

BACKGROUND: The effect of mitral regurgitation (MR) on the incidence of new cerebrovascular accidents (CVA) and mortality in patients with atrial fibrillation (AF) and left atrial thrombus (LAT) is unknown. OBJECTIVE: To investigate the effect of MR in patients with AF and LAT on new CVA and mortality. METHODS: Eighty nine consecutive patients, mean age 71 years, with AF and LAT documented by transesophageal echocardiography were investigated to determine the prevalence and severity of MR and the association of the severity of MR with new cerebrovascular accidents (CVA) and mortality at 34-mo follow-up. RESULTS: Of 89 patients, 1 + MR was present in 23 patients (26%), 2 + MR in 44 patients (50%), 3 + MR in 17 patients (19%), and 4 + MR in 3 patients (4%). Mean follow-up was 34 +/- 28 mo. The Cox proportional hazards model showed that the severity of increased MR did not significantly increase new CVA or mortality at 34-mo follow-up. The only variable predictive of mortality was left ventricular ejection fraction (LVEF), and with every unit increase in LVEF, the risk decreased by 3%. CONCLUSION: MR occurred in 87 of 89 patients (98%) with AF and LAT. There was no association between the severity of MR and the incidence of CVA or mortality.

Are the extent, location, and score of segmental wall motion abnormalities related to cardiac resynchronization therapy response?

BACKGROUND: We hypothesized that segmental wall motion abnormalities (WMAs) are related to cardiac resynchronization therapy (CRT) response. METHODS: We studied 108 patients who received CRT, 69 with ischemic and 39 with nonischemic heart disease. A wall motion score index (WMSI) was analyzed using a 17-segment model and calculated by the total score/number of segments analyzed. A decrease of left ventricular end systolic volume > or =15% after CRT was defined as a positive response to CRT. RESULTS: Of 108 patients, 1,054/1,836 segments (57%) had WMAs. The mean WMSI was 2.06 in patients with ischemic heart disease and 1.04 in patients with nonischemic heart disease (P < 0.0001). The area under the receiver operating characteristic curve for a WMSI predicting a positive response to CRT was 0.70 (P = 0.0001). The cutoff point was a WMSI < or =2 for prediction of a positive response to CRT. After adjustment for age, gender, and clinical features, the WMSI persistently related to CRT responders (P = 0.01). During 15-month follow-up, the percentage of CRT nonresponders in patients with a WMSI >2 was significantly higher (82%) compared to patients with a WMSI < or =2 (47%, P = 0.005) and nonischemic heart disease (36%, P < 0.001). In 59 patients with left ventricular mechanical dyssynchrony, the percentage of negative responders to CRT in patients with a WMSI >2, < or =2, and nonischemic heart disease were 53% (8 of 15), 16% (3 of 19) and 0% (0 of 25), respectively (P < 0.001). CONCLUSIONS: A large extent of WMAs and a WMSI >2 predicted a poorer CRT response.

Acute eosinophilic myocarditis mimicking myocardial infarction.

Eosinophilic myocarditis is characterized by progressive myocardial damage that results in heart failure and death. Herein, we present the case of a 54-year-old man who presented with symptoms of acute myocardial infarction. Normal coronary angiographic results and the presence of elevated levels of peripheral-blood eosinophilia prompted an endomyocardial biopsy that revealed acute eosinophilic myocarditis. The early initiation of steroid therapy resulted in the patient's substantial clinical improvement and survival. Early diagnosis of eosinophilic myocarditis and its treatment with steroid agents in some patients can lead to a favorable outcome. We discuss the challenge of diagnosing and identifying the characteristics of this variant of necrotizing eosinophilic myocarditis before the condition proves fatal.

Warfarin therapy initiated before is more beneficial than after transesophageal echocardiography detected left atrial thrombus.

OBJECTIVE: Warfarin anticoagulation significantly reduces the risk of thromboembolism in patients with atrial fibrillation (AF). However, there are many patients with AF who begin anticoagulation only after left atrial thrombus (LAT) is detected by transesophageal echocardiography (TEE). The impact of anticoagulation in these patients has not been clearly described. The purpose of this study was to investigate the incidence of cerebrovascular accident (CVA) among AF patients who began warfarin before LAT was detected by TEE compared to those who began warfarin only after TEE demonstrated LAT and those did not receive warfarin at any point. METHOD: Of the 90 consecutive AF patients with LAT (male 48, female 42, age 71.5 +/- 10.1 years), 49 began warfarin more than 3 weeks before TEE (Group I); 29 began warfarin after TEE (Group II); and 12 did not receive warfarin at all (Group III). RESULTS: The incidence of CVA in Group I (14%, 7/49, prior CVA 5, new CVA after TEE 2) was significantly lower than Group II (45%, 13/29, prior CVA 10, new CVA after TEE 3, P = 0.006) and III (42%, 5/12, prior CVA 3, new CVA after TEE 2, P = 0.047). Patients with persistent LAT had significantly higher incidence (64% vs 23%, P = 0.024) of CVA and lower CVA free survival than those with resolved LAT. CONCLUSION: The incidence of CVA among AF patients, who began warfarin before LAT detection, is significantly lower than those who began warfarin after LAT detection as well as those who did not receive warfarin at all.

Real-time three-dimensional echocardiography in diagnosis of right ventricular pseudoaneurysm after pacemaker implantation.

Right ventricular rupture is a critical cardiac complication associated with cardiac tamponade and death. Occasionally, the site of rupture may be contained by the parietal pericardium and thrombus, thus forming a pseudoaneurysm. Cases of traumatic pseudoaneurysm of the right ventricle have been reported. However, right ventricular pseudoaneurysm following pacemaker implantation has not been previously reported. This case demonstrates two right ventricular pseudoaneurysms following perforation of the right ventricular wall using real-time three-dimensional echocardiography (3DE) after pacemaker implantation although only one definite pseudoaneurysm was diagnosed by routine two-dimensional echocardiography (2DE). We also found that color Doppler 3DE enhanced visualization of the connections between the right ventricle and the pseudoaneurysm. Color Doppler 3DE allowed us to peel away the myocardial tissue and rotate the image to study the jets from different angles. In summary, real-time 3DE and color Doppler 3DE provided excellent visualization of the right ventricular pseudoaneurysm, flow between the ventricle and the pseudoaneurysm, and additional information to that obtained by 2DE.

Transesophageal echocardiography before cardioversion of recurrent atrial fibrillation: does absence of previous atrial thrombi preclude the need of a repeat test?

BACKGROUND: Atrial fibrillation (AF) is a recurrent problem that frequently requires repeat cardioversion. Transesophageal echocardiography (TEE) is indicated before cardioversion in patients who are underanticoagulated (warfarin therapy <3 weeks or international normalized ratio [INR] <2.0). It remains uncertain if TEE should be repeated in underanticoagulated patients who had no atrial thrombi detected by previous TEE. Methods and results From January 1996 to June 2001, 76 patients (43 men, 33 women; mean age, 68.8 +/- 10.4 years) who were underanticoagulated and had no atrial thrombi in previous TEE underwent repeat TEE before cardioversion of recurrent AF. The duration of recurrent AF at the time of the second TEE was 5.1 +/- 9.3 months (1 day to 4 years). The underlying diseases included coronary artery disease (n = 30), hypertension (n = 22), valvular heart diseases (n = 8), dilated cardiomyopathy (n = 4), hypertrophic cardiomyopathy (n = 2), and others (n = 10). Eight (10.5%) patients (2 men, 6 women; mean age, 68.6 +/- 6.6 years) were found to have intra-atrial thrombi on the second TEE. Of these 8 patients, 3 had coronary artery disease, 1 had hypertension, 2 had dilated cardiomyopathy, 1 had hypertrophic cardiomyopathy, and 1 had AF of unknown cause. The duration of recurrent AF in patients with and without thrombi was not significantly different (3.6 +/- 4.7 versus 5.3 +/- 9.7 months, P =.22). Of the 8 patients with intra-atrial thrombi on the second TEE, 5 had been taking warfarin for 3 to 4 weeks but had subtherapeutic INR and 3 were taking aspirin only. Compared with patients without intra-atrial thrombi, patients with intra-atrial thrombi had lower ejection fraction (32.5% +/- 18.1% versus 49.9% +/- 14.1%, P =.015), slower left atrial appendage empty velocity (0.22 +/- 0.08 versus 0.41 +/- 0.17 m/s, P <.01), and higher prevalence of spontaneous echo contrast (87.5%) than in patients without intra-atrial thrombi (19.1%, P <.05) but similar left atrial size (49.5 +/- 5.3 versus 47.3 +/- 7.1 mm, P =.15). Cardioversion was cancelled in all patients with atrial thrombi. CONCLUSIONS: In underanticoagulated patients, repeat TEE is necessary before cardioversion of recurrent AF even if the previous TEE showed no atrial thrombi.