2018 Vol. 15, No. 7
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2018, 15(7): 469-475.
doi: 10.11909/j.issn.1671-5411.2018.07.006
Abstract:
Objective Small coronary vessel disease (disease affecting coronary vessels with main branch diameters of ≤ 2.75 mm) is a common and intractable problem in percutaneous coronary intervention (PCI). This study was designed to test the theory that the effectiveness and safety of drug-eluting balloons for the treatment of de novo lesions in small coronary vessels are non-inferior to those of drug-eluting stents. Methods We designed a prospective, multicenter, randomized, controlled clinical trial aiming to assess the effectiveness and safety of the RESTORE? (Cardionovum, Bonn, Germany) drug-eluting balloon (DEB) versus the RESOLUTE? (Medtronic, USA) drug-eluting stent (DES) in the treatment of small coronary vessel disease. This trial started in August 2016. A total of 230 patients with a reference vessel diameter (RVD) ≥ 2.25 mm and ≤ 2.75 mm were randomly assigned to treatment with a DEB or a DES at a 1:1 ratio. The study was also designed to enroll 30 patients with an RVD ≥ 2.00 mm and ≤ 2.25 mm in the tiny vessel cohort. Results The key baseline data include demographic characteristics, relative medical history, baseline angiographic values and baseline procedural characteristics. The primary endpoint is in-segment diameter stenosis at nine months after the index procedure. Secondary endpoints include acute success, all-cause death, myocardial infarction, target vessel revascularization, target lesion revascularization and stent thrombosis. Conclusions The study will evaluate the clinical efficacy, angiographic outcomes, and safety of DEBs compared to DESs in the treatment of de novo coronary artery lesions in small vessels.
Objective Small coronary vessel disease (disease affecting coronary vessels with main branch diameters of ≤ 2.75 mm) is a common and intractable problem in percutaneous coronary intervention (PCI). This study was designed to test the theory that the effectiveness and safety of drug-eluting balloons for the treatment of de novo lesions in small coronary vessels are non-inferior to those of drug-eluting stents. Methods We designed a prospective, multicenter, randomized, controlled clinical trial aiming to assess the effectiveness and safety of the RESTORE? (Cardionovum, Bonn, Germany) drug-eluting balloon (DEB) versus the RESOLUTE? (Medtronic, USA) drug-eluting stent (DES) in the treatment of small coronary vessel disease. This trial started in August 2016. A total of 230 patients with a reference vessel diameter (RVD) ≥ 2.25 mm and ≤ 2.75 mm were randomly assigned to treatment with a DEB or a DES at a 1:1 ratio. The study was also designed to enroll 30 patients with an RVD ≥ 2.00 mm and ≤ 2.25 mm in the tiny vessel cohort. Results The key baseline data include demographic characteristics, relative medical history, baseline angiographic values and baseline procedural characteristics. The primary endpoint is in-segment diameter stenosis at nine months after the index procedure. Secondary endpoints include acute success, all-cause death, myocardial infarction, target vessel revascularization, target lesion revascularization and stent thrombosis. Conclusions The study will evaluate the clinical efficacy, angiographic outcomes, and safety of DEBs compared to DESs in the treatment of de novo coronary artery lesions in small vessels.
2018, 15(7): 476-478.
doi: 10.11909/j.issn.1671-5411.2018.07.002
Abstract:
Background Elevated NT-pro-BNP level has been identified as an independent predictor of mortality in heart failure and end stage renal disease. Previous studies diverge on NT-proBNP values predictive of mortality. The highest recorded NT-proBNP value in our institution is >70,000 pg/ml. No study to date has determined the association between a uniformly elevated NT-proBNP level and mortality. Methods Retrospective data from January 1, 2012 through January 30, 2016 was collected from patients with NT-proBNP>70,000 pg/ml. Mortality rate was determined via chart review or through the social security death index. Additional variables were gathered via systematic chart review. Results All-cause mortality was 45.39%, with a mean survival time of 204.1 days. There was a statistically significant difference in mortality (p=0.0089) and survival (p=0.0043) among patients with an ejection fraction 70,000 pg/ml, mortality rate is nearly 50%. Systolic heart failure with a left ventricular ejection fraction of <25% is a strong predictor of mortality in these patients.
Background Elevated NT-pro-BNP level has been identified as an independent predictor of mortality in heart failure and end stage renal disease. Previous studies diverge on NT-proBNP values predictive of mortality. The highest recorded NT-proBNP value in our institution is >70,000 pg/ml. No study to date has determined the association between a uniformly elevated NT-proBNP level and mortality. Methods Retrospective data from January 1, 2012 through January 30, 2016 was collected from patients with NT-proBNP>70,000 pg/ml. Mortality rate was determined via chart review or through the social security death index. Additional variables were gathered via systematic chart review. Results All-cause mortality was 45.39%, with a mean survival time of 204.1 days. There was a statistically significant difference in mortality (p=0.0089) and survival (p=0.0043) among patients with an ejection fraction 70,000 pg/ml, mortality rate is nearly 50%. Systolic heart failure with a left ventricular ejection fraction of <25% is a strong predictor of mortality in these patients.
2018, 15(7): 479-485.
doi: 10.11909/j.issn.1671-5411.2018.07.003
Abstract:
Objective Basic science studies demonstrated a general intramyocardial angiogenetic response potentially responsible for the creation of a microvascular neocapillaries network assisting myocardial function. We hypothesized that the benefit provided by the reperfusion of left anterior descending (LAD) territories and the biological angiogenetic drive triggered by the revascularization could translate in a global improvement in ventricular contractility, not restricted to the grafted area. Methods High-risk patients with multivessel coronary artery disease and preoperative wall motion abnormalities were retrospectively analysed to compare outcomes and regional ventricular function of those who received optimal medical therapy (OMT) versus those who underwent off-pump coronary artery bypass grafting (CABG) and received an incomplete myocardial revascularization using left internal mammary artery (LIMA) on LAD (off-pump CABG group). From January 2007 to December 2014, 206 patients (OMT n = 136, OPCAB n = 70) were propensity-score matched to have 70 matched pairs. Variables included in propensity score analyses were ejection fraction (EF), left ventricular end diastolic volume (LVEDVi), EuroSCORE II. Primary endpoint was the variation in the global wall motion score index (ΔWMSI) as evaluated by transthoracic echocardiography. Follow up was completed at 3 years from surgery or hospital discharge. Results Regional analysis of ventricular function revealed a regional WMSI improvement in the OPCABG group not only for LAD territories but also for non-LAD regions, associated with a reduction in the negative left ventricular ischemic remodeling, compared to patients discharged in optimal medical therapy. Global ΔWMSI was negative in OPCAB group (-3.4 ± 2.8%) and positive in the OMT group (5.9 ± 3.1%), indicating a better wall motion score for OPCAB patients. Surprisingly, regional WMSI improved also in non-grafted territories in the OPCAB group with a delta value of -3.7 ± 5.3% for left circumflex artery (LCX) area and -3.5 ± 5.4% for right coronary artery (RCA) area. Conclusions In patients with multivessel coronary artery disease, LIMA-to-LAD grafting is associated with an improvement in the WMSI involving also the surrounding non-LAD ungrafted segments and with the attenuation of negative global and regional ischemic ventricular remodelling.
Objective Basic science studies demonstrated a general intramyocardial angiogenetic response potentially responsible for the creation of a microvascular neocapillaries network assisting myocardial function. We hypothesized that the benefit provided by the reperfusion of left anterior descending (LAD) territories and the biological angiogenetic drive triggered by the revascularization could translate in a global improvement in ventricular contractility, not restricted to the grafted area. Methods High-risk patients with multivessel coronary artery disease and preoperative wall motion abnormalities were retrospectively analysed to compare outcomes and regional ventricular function of those who received optimal medical therapy (OMT) versus those who underwent off-pump coronary artery bypass grafting (CABG) and received an incomplete myocardial revascularization using left internal mammary artery (LIMA) on LAD (off-pump CABG group). From January 2007 to December 2014, 206 patients (OMT n = 136, OPCAB n = 70) were propensity-score matched to have 70 matched pairs. Variables included in propensity score analyses were ejection fraction (EF), left ventricular end diastolic volume (LVEDVi), EuroSCORE II. Primary endpoint was the variation in the global wall motion score index (ΔWMSI) as evaluated by transthoracic echocardiography. Follow up was completed at 3 years from surgery or hospital discharge. Results Regional analysis of ventricular function revealed a regional WMSI improvement in the OPCABG group not only for LAD territories but also for non-LAD regions, associated with a reduction in the negative left ventricular ischemic remodeling, compared to patients discharged in optimal medical therapy. Global ΔWMSI was negative in OPCAB group (-3.4 ± 2.8%) and positive in the OMT group (5.9 ± 3.1%), indicating a better wall motion score for OPCAB patients. Surprisingly, regional WMSI improved also in non-grafted territories in the OPCAB group with a delta value of -3.7 ± 5.3% for left circumflex artery (LCX) area and -3.5 ± 5.4% for right coronary artery (RCA) area. Conclusions In patients with multivessel coronary artery disease, LIMA-to-LAD grafting is associated with an improvement in the WMSI involving also the surrounding non-LAD ungrafted segments and with the attenuation of negative global and regional ischemic ventricular remodelling.
2018, 15(7): 486-491.
doi: 10.11909/j.issn.1671-5411.2018.07.005
Abstract:
Background The long-term prognostic influence of left atrial diameter (LAD) remodeling on the status of post-radiofrequency catheter ablation (RFCA) atrial fibrillation (AF) is unclear. This study employed a two-stage model from 3-year echocardiographic data to ascertain whether the two-stage model predicts RFCA outcome more favorably than models using the baseline LAD. Methods Data were retrospectively collected from 263 consecutive patients with drug-refractory AF undergoing RFCA. Regular echocardiographic measurements of LAD were performed at baseline, 1, 3, 6, and 12 months and then every 6 months after RFCA. Sex, age, type of AF, number of RFCA, and AF status were recorded. We obtain the actual (predicted) 3-year LAD using a longitudinal linear mixed model (1st stage). Logistic regression models based on the baseline LAD (Model 1), actual (predicted) 3-year LAD (Model 2) (2nd stage), and observed 3-year LAD (Model 3) were constructed to predict RFCA outcome. The area under the receiver operating characteristic curve (AUC) were used to assess the performance of models. Results The lowess smoothed curve indicated that the LAD declined over the first three months and remained stable up to 36 months after RFCA. The degree of LAD reduction was significantly influenced by the baseline LAD. Non-paroxysmal AF, large LAD and female gender were significant predictors of AF recurrence. Model 2 had the largest AUC among the three models. Conclusions This longitudinal study-based two-stage model outperforms the original logistic model using the baseline LAD. Non-paroxysmal AF, larger LAD and female gender are significant predictors of RFCA failure.
Background The long-term prognostic influence of left atrial diameter (LAD) remodeling on the status of post-radiofrequency catheter ablation (RFCA) atrial fibrillation (AF) is unclear. This study employed a two-stage model from 3-year echocardiographic data to ascertain whether the two-stage model predicts RFCA outcome more favorably than models using the baseline LAD. Methods Data were retrospectively collected from 263 consecutive patients with drug-refractory AF undergoing RFCA. Regular echocardiographic measurements of LAD were performed at baseline, 1, 3, 6, and 12 months and then every 6 months after RFCA. Sex, age, type of AF, number of RFCA, and AF status were recorded. We obtain the actual (predicted) 3-year LAD using a longitudinal linear mixed model (1st stage). Logistic regression models based on the baseline LAD (Model 1), actual (predicted) 3-year LAD (Model 2) (2nd stage), and observed 3-year LAD (Model 3) were constructed to predict RFCA outcome. The area under the receiver operating characteristic curve (AUC) were used to assess the performance of models. Results The lowess smoothed curve indicated that the LAD declined over the first three months and remained stable up to 36 months after RFCA. The degree of LAD reduction was significantly influenced by the baseline LAD. Non-paroxysmal AF, large LAD and female gender were significant predictors of AF recurrence. Model 2 had the largest AUC among the three models. Conclusions This longitudinal study-based two-stage model outperforms the original logistic model using the baseline LAD. Non-paroxysmal AF, larger LAD and female gender are significant predictors of RFCA failure.
2018, 15(7): 492-503.
doi: 10.11909/j.issn.1671-5411.2018.07.001
Abstract:
Background Ischemia/reperfusion injury (IRI) is an inflammatory response that occurs when tissue is reperfused following a prolonged period of ischemia. Several studies have indicated that C-reactive protein (CRP) might play an important role in inducing IRI. However, the effects of CRP on myocardial IRI and the underlying mechanisms have not been fully elucidated. This study aimed to investigate the association between CRP and myocardial IRI and the underlying mechanisms. Methods We simulated ischemia/reperfusion using oxygen-glucose deprivation/ reoxygenation (OGD/R) in neonatal Sprague-Dawley rat cardiomyocytes; reperfusion injury was induced by three hours of hypoxia with glucose and serum deprivation followed by one hour of reperfusion. Cell viability was tested with MTS assays, and cardiomyocyte damage was evaluated by lactate dehydrogenase (LDH) leakage. Mitochondrial membrane potential was measured using tetramethylrhodamine ethyl ester (TMRE) and mitochondrial permeability transition pore (mPTP) opening was measured using calcein/AM; both TMRE and caocein/AM were visualized with laser scanning confocal microscopy. In addition, we studied the signaling pathways underlying CRP-mediated ischemia/reperfusion injury via Western blot analysis. Results Compared with the simple OGD/R group, after intervention with 10 μg/mL CRP, cell viability decreased markedly (82.36 % ± 6.18% vs. 64.84% ± 4.06%, P = 0.0007), and the LDH leakage significantly increased (145.3 U/L ± 16.06 U/L vs. 208.2 U/L ± 19.23 U/L, P = 0.0122). CRP also activated mPTP opening and reduced mitochondrial membrane potential during myocardial ischemia/reperfusion. Pretreatment with 1 μM atorvastatin (Ator) before CRP intervention protected cardiomyocytes from IRI. Mitochondrial KATP channel opener diazoxide and mPTP inhibitor cyclosporin A also offset the effects of CRP in this process. The level of phosphorylated extracellular-signal-regulated kinase (ERK) 1/2 was significantly higher after pre-treatment with CRP compared with the OGD/R group (170.4% ± 3.00% vs. 93.53% ± 1.94%, P vs. 122.7% ± 5.30%, P = 0.0003) and ERK 1/2 phosphorylation significantly reduced after co-treatment with Ator and CRP compared with the level after CRP pretreatment alone. Conclusions Our results suggested that CRP directly aggravates myocardial IRI in myocardial cells and that this effect is primarily mediated by inhibiting mitochondrial ATP- sensitive potassium (mitoKATP) channels and promoting mPTP opening. Ator counteracts these effects and can reduce CRP-induced IRI. One of the mechanisms of CRP-induced IRI may be related to the sustained activation of the ERK signaling pathway.
Background Ischemia/reperfusion injury (IRI) is an inflammatory response that occurs when tissue is reperfused following a prolonged period of ischemia. Several studies have indicated that C-reactive protein (CRP) might play an important role in inducing IRI. However, the effects of CRP on myocardial IRI and the underlying mechanisms have not been fully elucidated. This study aimed to investigate the association between CRP and myocardial IRI and the underlying mechanisms. Methods We simulated ischemia/reperfusion using oxygen-glucose deprivation/ reoxygenation (OGD/R) in neonatal Sprague-Dawley rat cardiomyocytes; reperfusion injury was induced by three hours of hypoxia with glucose and serum deprivation followed by one hour of reperfusion. Cell viability was tested with MTS assays, and cardiomyocyte damage was evaluated by lactate dehydrogenase (LDH) leakage. Mitochondrial membrane potential was measured using tetramethylrhodamine ethyl ester (TMRE) and mitochondrial permeability transition pore (mPTP) opening was measured using calcein/AM; both TMRE and caocein/AM were visualized with laser scanning confocal microscopy. In addition, we studied the signaling pathways underlying CRP-mediated ischemia/reperfusion injury via Western blot analysis. Results Compared with the simple OGD/R group, after intervention with 10 μg/mL CRP, cell viability decreased markedly (82.36 % ± 6.18% vs. 64.84% ± 4.06%, P = 0.0007), and the LDH leakage significantly increased (145.3 U/L ± 16.06 U/L vs. 208.2 U/L ± 19.23 U/L, P = 0.0122). CRP also activated mPTP opening and reduced mitochondrial membrane potential during myocardial ischemia/reperfusion. Pretreatment with 1 μM atorvastatin (Ator) before CRP intervention protected cardiomyocytes from IRI. Mitochondrial KATP channel opener diazoxide and mPTP inhibitor cyclosporin A also offset the effects of CRP in this process. The level of phosphorylated extracellular-signal-regulated kinase (ERK) 1/2 was significantly higher after pre-treatment with CRP compared with the OGD/R group (170.4% ± 3.00% vs. 93.53% ± 1.94%, P vs. 122.7% ± 5.30%, P = 0.0003) and ERK 1/2 phosphorylation significantly reduced after co-treatment with Ator and CRP compared with the level after CRP pretreatment alone. Conclusions Our results suggested that CRP directly aggravates myocardial IRI in myocardial cells and that this effect is primarily mediated by inhibiting mitochondrial ATP- sensitive potassium (mitoKATP) channels and promoting mPTP opening. Ator counteracts these effects and can reduce CRP-induced IRI. One of the mechanisms of CRP-induced IRI may be related to the sustained activation of the ERK signaling pathway.
2018, 15(7): 504-512.
doi: 10.11909/j.issn.1671-5411.2018.07.007
Abstract:
Hypertensive crises are elevations of blood pressure higher than 180/120 mmHg. These can be urgent or emergent, depending on the presence of end organ damage. The clinical presentation of hypertensive crises is quite variable in elderly patients, and clinicians must be suspicious of non-specific symptoms. Managing hypertensive crises in elderly patients needs meticulous knowledge of the pathophysiological changes in them, pharmacological options, pharmacokinetics of the medications used, their side effects, and their interactions with other medications. Clevidipine, nicardipine, labetalol, esmolol, and fenoldopam are among the preferred choices in the elderly due to their efficacy and tolerability. Nitroprusside, hydralazine, and nifedipine should be avoided, unless there are no other options available, due to the high risk of complications and unpredictable responses.
Hypertensive crises are elevations of blood pressure higher than 180/120 mmHg. These can be urgent or emergent, depending on the presence of end organ damage. The clinical presentation of hypertensive crises is quite variable in elderly patients, and clinicians must be suspicious of non-specific symptoms. Managing hypertensive crises in elderly patients needs meticulous knowledge of the pathophysiological changes in them, pharmacological options, pharmacokinetics of the medications used, their side effects, and their interactions with other medications. Clevidipine, nicardipine, labetalol, esmolol, and fenoldopam are among the preferred choices in the elderly due to their efficacy and tolerability. Nitroprusside, hydralazine, and nifedipine should be avoided, unless there are no other options available, due to the high risk of complications and unpredictable responses.
2018, 15(7): 513-516.
doi: 10.11909/j.issn.1671-5411.2018.07.008
Abstract:
Although the majority of diabetic patients with myocardial infarction have angiographic evidence of significant coronary artery disease, they can also experience myocardial infarctions with non-obstructive coronary arteries (MINOCA). We present the case of a 72 years old diabetic and hypertensive woman admitted for progressive dyspnoea. She affirmed long-term moderate effort retrosternal pain, resolving with rest. Clinically there were congestive heart failure signs. ECG showed sinus tachycardia, ST segment elevation in leads V1-V5 and biphasic T waves V4-V6. Cardiac necrosis markers were slightly elevated and echocardiography revealed akinetic interventricular septum, severe global left ventricular dysfunction (left ventricular ejection fraction – LVEF – of 35%) with elevated filling pressures. Coronary angiography did not show any significant stenosis, but during the procedure a significant left anterior descending coronary artery spasm was registered. Under medical treatment ST elevation resolved, LVEF increased to 45% in a week. Starting 10-th day after admission the patient developed symptomatic sinus bradycardia, sinus pauses, isorhythmic atrio-ventricular dissociation and junctional escape rhythm. After beta blockers were stopped, the conduction disturbances did not improve and patient received a DDDR pacemaker. Our final diagnosis was MINOCA due to coronary spasm and microvascular coronary dysfunction, in an uncontrolled diabetic and dyslipidemic patient. The conduction disturbancies needing permanent cardiac pacing seemed to be due to a latent sinus node dysfunction unmasked by beta blockers administration. MINOCA has several possible etiologies, sometimes atypical evolution and poses many challenges to the practitioner.
Although the majority of diabetic patients with myocardial infarction have angiographic evidence of significant coronary artery disease, they can also experience myocardial infarctions with non-obstructive coronary arteries (MINOCA). We present the case of a 72 years old diabetic and hypertensive woman admitted for progressive dyspnoea. She affirmed long-term moderate effort retrosternal pain, resolving with rest. Clinically there were congestive heart failure signs. ECG showed sinus tachycardia, ST segment elevation in leads V1-V5 and biphasic T waves V4-V6. Cardiac necrosis markers were slightly elevated and echocardiography revealed akinetic interventricular septum, severe global left ventricular dysfunction (left ventricular ejection fraction – LVEF – of 35%) with elevated filling pressures. Coronary angiography did not show any significant stenosis, but during the procedure a significant left anterior descending coronary artery spasm was registered. Under medical treatment ST elevation resolved, LVEF increased to 45% in a week. Starting 10-th day after admission the patient developed symptomatic sinus bradycardia, sinus pauses, isorhythmic atrio-ventricular dissociation and junctional escape rhythm. After beta blockers were stopped, the conduction disturbances did not improve and patient received a DDDR pacemaker. Our final diagnosis was MINOCA due to coronary spasm and microvascular coronary dysfunction, in an uncontrolled diabetic and dyslipidemic patient. The conduction disturbancies needing permanent cardiac pacing seemed to be due to a latent sinus node dysfunction unmasked by beta blockers administration. MINOCA has several possible etiologies, sometimes atypical evolution and poses many challenges to the practitioner.
2018, 15(7): 517-518.
doi: 10.11909/j.issn.1671-5411.2018.07.009
Abstract:
Myocarditis is an inflammatory disease of the myocardium. The clinical presentation of myocarditis may range from subclinical to sudden death. The incidence of fatal myocarditis, which often presents with sudden or rapid death, has been estimated at 0.15/100.000 in the general population and is highest in infants and young adults (but may affect any age group). However, diffuse myocarditis in autopsies of sudden death is < 2% in adult. Myocarditis usually presents with heart failure symptoms over a few days to weeks. The classic presentation of viral myocarditis includes a viral prodrome with fever, myalgia, and upper respiratory symptoms. Patients present with dyspnea, chest pain, and arrhythmias. ECG abnormalities are often present, along with evidence of myocardial damage with elevated troponin levels. We present the case of a 78 year old white male who died from acute cardiac decompensation from diffuse acute lymphocytic myocarditis. A 78 year old white male with a medical history of hypertension and asbestosis who presented to the emergency department with agitation and wide complex tachycardia after three nights of difficulty sleeping, shortness of breath and diaphoresis. Patient required emergent intubation for hypoxic respiratory failure. An ECG performed at the time of admission was read as possible STEMI and the patient was taken to the cardiac catheterization lab. The procedure found open and patent coronary vasculature within the exception of occlusion of a branch of the second obtuse marginal artery branching from the left circumflex artery which was treated with a Plain Old Balloon Angioplasty (POBA). During the same day, patient went into cardiac arrest and deceased. An autopsy, the major pathological findings that explain the patient’s terminal course were in the heart which was affected by extensive diffuse myocarditis, predominantly lymphocytic with associated myocyte necrosis and dilated cardiomyopathy. The inflammation is more marked in the left than the right ventricle and is also involving the papillary muscles, endocardium and focally the epicardium. Scarring with dystrophic calcification in addition to the inflammation is present at the atrioventricular-septal junction (AV node site). Inflammation is also focally present at the junction of right atrium and superior vena cava (SA node site). Myocardial scar tissue from remote infarction or chronic ischemia is present in the inner lateral wall of the left ventricle. In this case, the predominance of lymphocytic infiltrate in myocarditis without neutrophil microabscesses, prominent eosinophils, giant cells or granuloma is most consistent with the differential etiology of viral/postviral infection, autoimmune/connective tissue disease or idiopathic.
Myocarditis is an inflammatory disease of the myocardium. The clinical presentation of myocarditis may range from subclinical to sudden death. The incidence of fatal myocarditis, which often presents with sudden or rapid death, has been estimated at 0.15/100.000 in the general population and is highest in infants and young adults (but may affect any age group). However, diffuse myocarditis in autopsies of sudden death is < 2% in adult. Myocarditis usually presents with heart failure symptoms over a few days to weeks. The classic presentation of viral myocarditis includes a viral prodrome with fever, myalgia, and upper respiratory symptoms. Patients present with dyspnea, chest pain, and arrhythmias. ECG abnormalities are often present, along with evidence of myocardial damage with elevated troponin levels. We present the case of a 78 year old white male who died from acute cardiac decompensation from diffuse acute lymphocytic myocarditis. A 78 year old white male with a medical history of hypertension and asbestosis who presented to the emergency department with agitation and wide complex tachycardia after three nights of difficulty sleeping, shortness of breath and diaphoresis. Patient required emergent intubation for hypoxic respiratory failure. An ECG performed at the time of admission was read as possible STEMI and the patient was taken to the cardiac catheterization lab. The procedure found open and patent coronary vasculature within the exception of occlusion of a branch of the second obtuse marginal artery branching from the left circumflex artery which was treated with a Plain Old Balloon Angioplasty (POBA). During the same day, patient went into cardiac arrest and deceased. An autopsy, the major pathological findings that explain the patient’s terminal course were in the heart which was affected by extensive diffuse myocarditis, predominantly lymphocytic with associated myocyte necrosis and dilated cardiomyopathy. The inflammation is more marked in the left than the right ventricle and is also involving the papillary muscles, endocardium and focally the epicardium. Scarring with dystrophic calcification in addition to the inflammation is present at the atrioventricular-septal junction (AV node site). Inflammation is also focally present at the junction of right atrium and superior vena cava (SA node site). Myocardial scar tissue from remote infarction or chronic ischemia is present in the inner lateral wall of the left ventricle. In this case, the predominance of lymphocytic infiltrate in myocarditis without neutrophil microabscesses, prominent eosinophils, giant cells or granuloma is most consistent with the differential etiology of viral/postviral infection, autoimmune/connective tissue disease or idiopathic.
