The Transmural Dispersion Of Repolarization Characteristics Of Acute Myocarditis And Correlation Study Between NT-Pro-B-Type Natriuretic Peptide

BackgroundNotion and historyViral myocarditis is a common disease of Cardiology caused by a viral infection, which consists of focal or diffuse myocardial damage. Since the the first outbreak of viral myocarditis in China at 1970s, Japan and other countries also has continued to grow, and since then, much attention concerning on viral myocarditis have also been reported. Although the first current of viral myocarditis have passed decades, however, the mechanism of the disease so far is not entirely clear. Therefore, Europe and the United States has also invested more attention on this disease. With the tremendous advances in molecular biology in recent years, although there is no breakthrough, people’s understanding of viral myocarditis there is a great improvement. Because the disease spectrum changes and evolution of the virus, viral diseases is also increasing. Viral myocarditis has becoming a more common diseases. Expected to be a common disease in the 21st century, the incidence of viral myocarditis will develop secondery place,after to coronary heart disease Therefore, to master the viral epidemiology and diagnosis has a very important role.Epidemiology of VMCViral myocarditis can occur in all ages, from infants to the elderly person. But it occurs mainly in children and adults less than 40 years of age, about 35%of patients between 10 and 30 years old. Because the variety of VMC viruses and their epidemic law, there are differences between different regions and in different years within the same region in the predominant viruses.Virus spectrumMany viruses can cause viral myocarditis, it has reported at least 30 kinds of viruses can cause myocarditis infection. Among intestinal virus Coxsackie (Coxsackie), group A、B are the most common type, especially Coxsackie B-2-6,9 and A-9 virus. Second is ECHO viruses, especially type 6. next, all types of adenovirus type 3. Especially Coxsackie B type virus (CVB) accounts for 30-50% of the number of patients with viral myocarditis. In addition, polio virus, influenza virus,, rubella virus, herpes simplex virus, encephalitis virus, hepatitis viruses (A, B, C type), and HIV and other viruses also can cause myocarditis.1.4Clinical Presentation of VMCClinical manifestations of viral myocarditis depends on the extent of disease, ranging from asymptomatic to cardiac sudden death. About half patients has prodromal symptoms 1-3 weeks before the onset of viral infection, such as fever, general malaise, the so-called "cold" like symptoms or nausea, vomiting and other gastrointestinal symptoms. Then palpitations, chest pain, dyspnea, edema, and even Adams-Stokes syndrome. Physical examination could found tachycardia that is not parallel to the heating degree, arrhythmia, third heart sound or noise. Or jugular vein distention, rales lungs, liver and other signs of heart failure. Severe patients can occur cardiogenic shock.1.5Auxiliary examinationsChest X-ray:podoid enlargement.ECG:ST-T segment changes, low voltage, QRS axis abnormalities, QT prolonged, abnormal Q waves, branch/atrioventricular block and additional contraction. In general, abnormal ECG changes observed during the process of myocarditis. ECG manifestations are various, including atrioventricular block (I-III degree), intraventricular conduction delay (wide QRS complex), R-wave amplitude reduction, abnormal Q waves, ST-T segment changes, low voltage, frequent premature beats, supraventricular tachycardia, atrial fibrillation,sinus arrest,ventricular tachycardia, ventricular fibrillation, and asystole.Echocardiogram:Cardiac dysfunction, pericardial effusion. No specific echocardiographic features of myocarditis. However, echocardiography can be evaluated heart chamber size and wall thickness, systolic and diastolic function. The evaluation of different parameters have some relevance with prognosis. Fulminant myocarditis patients usually with normal cardiac chamber size,but increased septal thickness if secondary to acute myocardial edema, and acute myocarditis patients with significant left ventricular dilation and wall thinning localized or diffuse, wall motion, echocardiography chart can be found in the pericardial effusion.AST, CPK, LDH, etc. rise in the early stage. In myocarditis, myocardial constitutive proteins (cardiac troponin T and creatine kinase-MB) are detected in serum. C-reactive protein and white blood cell count are elevated. Early detection of troponin T using whole blood enables immediate diagnosis of myocarditis, but normal values do not exclude an acute myocardial inflammatory process.Viral antibody:Polymerase chain reaction is often used to demonstrate the presence of viral infection and to detect the viral genome. Within 3 weeks after onset, the two serum CVB neutralizing antibody was increased four times or more if two weeks apart, or one up to 1:640, alien CVB IgM 1:320 above (according to different laboratory standard), peripheral blood leukocyte positive intestinal virus nucleic acid, etc., are the causes of some possible but not sure diagnosis index. Separation of virus or identification of virus by antibody titer in throat swabs, urine, feces,blood, and especially pericardial effusion or cardiac muscle tissue provides direct evidence of myocarditis.Diagnosis of MyocarditisBecause of the various symptoms and conditions, the non-specific symptoms and auxiliary examinations, It’s difficult to make a diagnosis of VMC without a unified international standard. clinical diagnosis index of VMC" was first prompted in the 1970s in China. the present diagnostic standard of pediatric myocarditis was refined at the Pediatrics Myocarditis and Cardiomyopathy conference in September 1999.Gold standard of diagnosis:Endomyocardial biopsy.Endomyocardial biopsy (EMB) is considered as the"gold standard" for VMC diagnosis, and also forms the basis for histology diagnosis. However, it is an invasive examination whose safety remains to be evaluated,which limits its clinical application. The inconsistencies in sampling time, region error and diagnosis standard limit the accuracy of the diagnosis.Currently, in clinical, the diagnosis of myocarditis often is the combination of comprehensive judgments of history, clinical presentation, ECG, echocardiography, biochemical tests (blood, CK-MB, troponin I or T, C-reactive protein, virus antibodies). In the present study, Oclussion other cardiomyopathy,the diagnostic of myocarditis reference 7th edition Internal Medicine standard:(1) before the onset of 1-3 weeks have clear history of precursor infection; (2) the ecg has the characteristics of myocardial injury, or at least more than one arrhythmia; (3) with chest pain, chest tightness, or low cardiac output or the performance of the heart failure; (4) in the course of the disease has increased myocardial injury biomarkers or echocardiographic refer dilated or confirm decreased left ventricular systolic or diastolic function. With the above four for at least two or more. In this study,32.5% patients has been confirmed with acute myocardial infarction by coronary angiography.Treatment of MyocarditisIn acute myocarditis, avoidance of aerobic physical activity is indicated in addition to pharmacological therapy. Standard HF regime including beta-blockers,diuretics,angiotens inconvert ingenzyme (ACE) inhibitors or angiotensin-Ⅱ receptor lockers (ARBs) should be initiated according to the New ork Heart Association (NYHA) functional class. Temporarypacemaker insertion is indicated for patients with acute myocarditis who present with symptomatic atrioventricular(AV) block Ⅱ or Ⅲ. The rationale to use immunoglobulin in viral myocarditis results from their antiviral and immunomodulating effects. Treatments with immunosuppressive agents (cyclosporine, prednisolone, azathioprine)in acute myocarditis have shown controversial results.Prognosis and OutcomeMost patients can be cured after treatment, but often occurs arrhythmia, especially each type of contraction, but also can develop into atrioventricular block, in more serious cases, a small number of patients in the acute phase may be death due to serious heart rhythm disorders, acute heart failure and cardiogenic shock. After a period of time some patients may appear enlarged heart, heart dysfunction, with or without arrhythmias or ECG abnormalities, it is difficult to identify with dilated cardiomyopathy.As everyone knows, a lot of cause could reduce local or diffuse myocardial injury, such as myocardial ischemia and hypoxia, inflammation.myocardial damage can be caused a series of changes in biochemical markers. For example, as introduced in front,changes of cardiac troponin (T and I), myocardial creatine kinase (CK-MB), erythrocyte sedimentation rate and acute phase proteins or hypersensitivity reaction of acute phase protein (C reactive protein and high-sensitivity C reactive protein changes) etc.The damage of viral myocarditis, not only cause the change of the biochemical markers but also cause changes on electrocardiographic. The electrocardiology including the polar and bipolar. In recent years, many study found that some index of repolarizion, such as QT interval, T wave the peak to the end interval,it may predict the occurrence of malignant ventricular arrhythmia in acute myocardial infarction, hypertrophy cardiomyopathy obstruction type, dilated cardiomyopathy, heart failure, early repolarization syndrome and other diseases.In the process of acute viral myocarditis,it is prone to various arrhymias,such as tachycardia, atrioventricular block, premature beat etc. especially ventricular tachycardia and ventricular fibrillation is easy to cause the hemodynamic instability,it is very dangerous. Therefore, myocarditis has a high mortality, and become a severe disease of cardiovascular. As described front, the dispersion repolarizion can predict the occurrence arrhythmias in many diseases, and reflect the prognosis of patients.There are many biological indicators to assess the severity of myocardial of viral myocarditis, the increased in serum troponin T or I), myocardial enzyme creatine (CK-MB), blood sedimentation, high-sensitivity c-reactive protein may help the diagnose.much biological and biochemical factors can damage to the heart cells, its metabolites inosine the damage to the kidney and heart; Acute occlusion of coronary artery reduced hypoxia of myocardial ischemia; Carbon monoxide damage on myocardial cells. Myocardial cell injury will affect the electrocardiology of myocardial. Viral myocarditis is endocardial inflammation caused by viral infections. Infection would cause damage on myocardial. QT interval reperezente lectrophysiological stability of uremic cardiomyopathy, electrocardiogram (ecg) is a very simple and common examination in clinical, thus we made a bold assumption, electrocardiogram (ecg) index can response the electrophysiological stability of the viral myocarditis s? But at the moment predictor occurres of cardiac arrhythmias of viral myocarditis electrocardiology is still missing.OBJECTIVEThis study select the patients with acute viral myocarditis in nanfang hospital cardiovascular medical intensive care unit (CCU) as the object group, and divided all subjects into arrhythmia group and noarrhythmia group, selected paroxysmal supraventricular tachycardia patients nearly the same age, gender and sex (but at the time or after a short tachycardia has terminated) as a normal control group. Measure the period of QT interval, T wave peak to end of two group.collection biochemical markers of two groups. Through analysis and comparison electrocardiogram (ecg) and the biochemical marker of two groups patients, to clarify the dispertion repolarizion of patients with acute viral myocarditis, and clarify the correlation between pro-BNP.3. Materials and methods3.1 The object of studyRetrospectively collected patients in cardiovascular medical intensive care unit (CCU) of nanfang hospital between September 2012 and September 2012, a total of 80 patients with acute myocarditis were selected as experimental group, men,52 cases, women,28 cases, aged from 8-63 (30.850±13.122). collected 78 cases (male cases, female patients, ages11-63Age (35.350±13.322) in the clinical pathway, but sex and age nearly matched patients as control group, and no tachycardia attack at that time (note:in cases of clinical pathway it is the conventional to measurement myocardial injury biomarkers, nauretic peptide). Oclussion other cardiomyopathy,the diagnostic of myocarditis reference 7th edition Internal Medicine standard:(1) before the onset of 1-3 weeks have clear history of precursor infection; (2) the ecg has the characteristics of myocardial injury, or at least more than one arrhythmia; (3) with chest pain, chest tightness, or low cardiac output or the performance of the heart failure; (4) in the course of the disease has increased myocardial injury biomarkers or echocardiographic refer dilated or confirm decreased left ventricular systolic or diastolic function. With the above four for at least two or more. In this study,32.5% patients has been confirmed with acute myocardial infarction by coronary angiography. Exclusion criteria:(1) the patients stay at recovering or sequela period; (2) in the acute stage, but has been treated outside for more than one day; (3) suspected myocarditis but coronary angiography vessels with different degree of stenosis. All the research object through the history and physical examination, electrocardiogram, ultrasonic doppler, electrocardiogram, electrolytes, liver function, chest X-ray, kidney, plate movement tests or coronary artery angiography revealed no abnormalities, without cardiovascular disease, or may cause abnormal electrocardiogram, and rule out all kinds of structural heart disease, ischemic cardiomyopathy, hereditary ion channel disease (including Brugada syndrome, long QT syndrome, short QT syndrome, catecholamine sensitivity polymorphous ventricular tachycardia, etc.), cardiomyopathy (including arrhythmogenic right ventricular cardiomyopathy).3.2 Data Go to electronic medical records system at department of cardiovascularology in nanfang hospital and collect two group of patients with basic information such as gender, age, collect all information of viral myocarditis include myocardial injury biomarkers (troponin, CK-MB), nauretic peptide (BNP), to the record room of nanfhag hospital, measure the information on the electrocardiogram (ecg) of patients’heart rate,QTinterval, T wave peak to end interval, etc..3.3.1 measurement on heart rate:measure the number of small grid of two adjacent QRS waves on electrocardiogram (ecg), using 1500/small grid calculation method;when encounter arrhymias such as atrial fibrillation, premature contraction, count the QRS wave number of10 seconds on electrocardiogram, and then multiplied six.3.3.2 measurement of QT interval:measure the starting point of QRS complex wave, end point of T wave is defined as the decline of T wave and the intersection point of the baseline, when encounter premature contraction then measure the QT period before the contract or after premature contraction. If an occasional fusion of premature ventricular beats and sinus rhythm, still treatment by premature contraction.3.3.3 measurement of Tp-Te interval:take the distance from T peak to T end. when encounter premature contraction then measure the QT period before the contract or after premature contraction. If an occasional fusion of premature ventricular beats and sinus rhythm, still treatment by premature contraction.3.4 StatisticsUsing SPSS 13.0 statistical software package, to adopt method Means+SD on categorical data, comparison the two groups of independent sample by t test. Bivariate correlation between using Pearson correlation test. The P value less than 0.05 then consider the difference was statistically significant.4. Results The results of the experimental group and control group the statistical results of the basic information of two groups such as age, nauretic peptide, electrocardiogram (ecg) index is as follows (table 1).4.1The comparison of the basic information patients with acute viral myocarditis as experimental group, a total of 80 cases, men,52 cases; women,28 cases, the youngest is 8 years old, the eldest is 63 years old; the "normal" people with supraventricular tachycardia but not attack as control group, a total of 78 cases, men38 cases, women,40cases. the youngest is 1 lyears old, the eldest is 63 years old; The comparesion of experimental group between control group, two groups were comparable in terms of basic information, between the two groups there have no obvious differences in terms of age (p= 0.154). The experimental group and control group there was no statistically significant difference in heart rate (p=0.296).4.2 The comparesion for experimental group and control group the experimental group had hightert troponin than control group, differences between the two groups was statistically significant (p=0.000) (20.423+/-18.857 VS0.422+/-0.780). And experimental nauretic peptide level is significantly higher than control, difference was obvious (p=0.003) (6800.179+/-10066.241 VS510.845+/-974.718). in the experimental group Tp-Te interval range from84-138 ms, the control group Tp-Te from54-140ms. Experimental group compared with control group, the experimental Tp-Te interval is largeer, has statistically difference (p= 0.004) (109.525+/-15.458 VS98.179+/-18.307) (table 1). QT interval is a slight difference between the two groups, but has not yet reached statistical significance (p= 0.171) (364.925+/-53.732 VS380.359+/-45.100).4.3 Arrhythmia subgroup analysis of the experimental group patients with acute viral myocarditis, arrhythmia subgroup compare to noarrhythmia subgroup, Tp-Teinterval have no statistical significance between the two subgroups (p= 0.942); in terms of troponin and QT no statistically difference were observed between arrhythmia subgroup and noarrhythmia subgroup, p values were 0.262 and 0.078 respectively. But the BNP level between the two subgroups was statistical significance (p= 0.046), BNP levels increased significantly in arrhymia subgroup than noarrhythmia subgroup (12641.080+/-3544.709 VS3614.230+/-5745.034) (table 2).4.4 Correlation analysis Of the Pearson correlation test in experimental group with acute viral myocarditis between Tp-Te interval and BNP, there was no correlation (r=0.201, p=0.201).5. Conclusion1, Patients with acute viral myocarditis has relatively higher Tp-Te interval than healthy people, poor heart electricity stability, easy occurrence arrhythmia;2, Acute viral myocarditis between arrhythmia and noarrhythmias has no obvious difference in Tp-Te interval, but patients appeared arrhythmia with higher BNP levels;3, Between Tp-Te and BNP level in viral myocarditis patients, and there was no obvious correlation between the BNP level.