| Background and PurposeVentricular septal rupture(VSR)is a likely mortal complication of acute myocardial infarction(AMI).In the stage of efficient reperfusive therapies(either pharmacological or mechanical),the prevalence of VSR has substantially diminished.However,the fatality among patients with AMI with VSR is noted as high as 80%indeed in new sequence of cases with AMI undergoing immediate percutaneous coronary intervention(PCI),and appears relatively unaffected over the last few decades.Prior to the use of thrombolysis and percutaneous coronary intervention(PCI),the proportion of VSR after AMI was as high as 1-3%.After reperfusion remedies became the ideal of action in the management of AMI,the prevalence of VSR decreased to 0.170.31%.However,despite the advancements in quick diagnosis and treatment of both AMI and VSR,the fatality percentage from VSR remains extremely high ranging from 45-80%.As was shown in the SHOCK trial and approved by GUSTO-I and APEXAMI,VSR typically takes place much earlier ranging from 8-24 hours after AMI and answered not significantly differ in those taking thrombolysis from those who did not.However,the advanced prompt detection of VSR maybe the result of other factors including near common access to echocardiography and modifications in tissue pathology as a result of reperfusion injury coupled with fibrinolysis.Despite improvements and promising results in non-surgical managements of VSR such as transcatheter closure strategies,surgical repair of septal defects remain the mainstay of treatment.Current guidelines from the American College of Cardiology Foundation and American Heart Association(ACCF/AHA)recommend emergent surgical repair regardless of hemodynamic stability at the time of diagnosis.Despite professional understanding on the necessity of surgical repair,the timing of VSR repair and perioperative therapeutic management remains controversial.This study will evaluate the VSR site and size with particular appeal to its relationship to the severity of heart failure.Materials and MethodsStudy design and patient selectionA retrospective analysis was performed on 71 consecutive patients with VSR following AMI who presented or transferred to the first affiliated hospital of Zhengzhou University between the January 2012 and December 2018.A total of 4 patients were transferred from outside facilities with only 1 having prior diagnosis of VSR obtained at the presenting hospital.Inclusion criteria were any patient admitted for AMI who had emergent cardiac catheterization with evidence of VSR or had hemodynamic compromise with echocardiographic evidence of VSR.Patients who died on initial presentation were excluded,including those who were taken for emergent cardiac catheterization but did not survive.Diagnosis of AMI was made based on clinical symptoms and elevation of serum troponin-T>0.1 mg/dL with or without electrocardiogram(ECG)evidence of>2 mm ST-segment elevation in the precordial leads or>1 mm ST-segment elevation in the limb leads.We completed a thorough chart review and analysis of the clinical profile,treatments including medical and surgical,and outcomes of all patients.The earliest recorded vital signs were used to determine the clinical hemodynamics for each case.Cardiac catheterizationAfter diagnosis of AMI in the emergency department,all patients were taken for emergent heart catheterization(HC)All patients received coronary angiogram with the intention to perform primary intervention.Some patients also had left ventriculogram prior to echocardiographic confirmation.Coronary artery disease(CAD)was defined based on the degree of obstruction.No apparent CAD was defined as no stenosis greater than 20%.Non-obstructive CAD included at least 1 or more lesions with stenosis greater than 20%but less than 70%.Obstructive CAD was defined as any stenosis greater than 70%or left main stenosis greater than 50%with a distribution involving 1,2 or 3 vessels.EchocardiographyAll patients underwent an echocardiogram with confirmation of VSR by transthoracic and/or transesophageal methods within an average of 4 hours and 36 minutes of hospital admission(maximum 13 hours and 51 minutes).Diagnosis of VSR was defined as disruption in the ventricular septum with evidence of left-to-right shunt by color Doppler.The location of the VSR was identified via transthoracic echocardiogram(TTE).VSR location was recorded as apical septum,mid septum.Left ventricular ejection fraction(LVEF)was calculated by either the Quinonez method or the biplane Simpson's method.VariablesThe demographic characteristics,medical co-morbidities(smoking history,hypertension,diabetes mellitus,previous cerebrovascular accident,and renal function),medical acuity(prodromal angina,left ventricular ejection fraction(LVEF),and Killip classification,NYHA classification),the location of infarction,site and size of septal rupture,and the peak cardiac enzymes were obtained by chart review.Prodromal angina was defined as typical chest pain episodes(either at rest or upon effort)persisting<30 minutes and occurring within 24 hours before the onset of the AMI.The use of early PCI(?6 hours after AMI),intra-aortic balloon pump(IABP),concomitant surgical procedures,and calendar year of operation were also included as variables for analysis.Outcomesoutcomes were the indicators of severity of heart failure,defined as factors that can predict he severity of heart failure based on the clinical classification of cardiac failure and statistical analysis.The New York Heart Association classification of heart failure(Table 1)can be used to describe the severity of heart failure,the symptoms of heart failure and limitation of exercise capacity,and is useful to assess response to therapy.Statistical analysisContinuous variables were summarized as mean plus/minus the standard deviation(SD).Categorical variables were expressed as percentage of the sample.Comparison between apical VSR versus middle VSR was performed by independent sample test(Whitney U test)and the Chi-square test using Yates correction and Fisher's exact test for continuous and categorical variables respectively.A two tailed p-value less than 0.05 was used to indicate statistical significance.ResultsA total of 71 subjects were diagnosed with VSR after MI between the years of 2012-2018.The mean age±standard deviation(SD)was(66.2±8.88)years old with(n=36,50.7%)were males and(n=35,49.3%)were females gave rise to(M:F)ratio almost equal(1.02:1).Forty patients(56.3%)had diabetes mellitus which was common risk factor of post myocardial infarction VSR,followed by hypertension which found in(n=33,46.5%).Twenty six patients(36.6%)were on dialysis.Smoking and history of cerebrovascular accident were presented in 14 patients(19.7%),and 7 patients(9.9%)respectively.HDL was low in 21 patients(29.6%)and LDL was high in 17 patients(23.9%).(Table 2).Twenty five patients(35.2%)were supported by IABP and(n=19,26.8%).The majority of patients at the time of diagnosis of AMI were Killip class ?(n=33,46.5%)or class ?(n=20,28.2%).Extensive anterior(n=31,43.7%)and anterior(n=26,36.6%)myocardial infarctions were the most common location of myocardial infarction.The apical VSR(n=49,69.0%)was the most common VSR location,while there were 22 patients(31.0%)with the middle VSR.The average LVEF was(48.5±10.4%).A coronary angiogram was completed in all patients with unequal number of patients divided into 1-,2-,or 3-vessel disease categories.Left anterior descending coronary artery(LAD)was the most common location for culprit lesions at(n=60,84.5%)followed by the right coronary artery(RCA)at(n=9,12.7%).Revascularization procedure was performed in 65 patients.Among them(n=40,56.3%)patients received PCI and(n=57,80.3%)received thrombolysis.(Table 3).From table 4,age,gender,killip class,NYHA class and Pro-BNP were not significantly different between apical VSR group and middle VSR group.The apical VSR group had a lower LVEF than the middle VSR group(46.08±8.88%vs.53.36±11.72%,p=0.012),a lower LVEF predicted a severe heart failure.There was a significant difference in the size of the VSR among the two groups which was smaller in the apical group than that in the middle one(7.51±3.37mm vs.10.77±5.97mm,p=0.016).The location of the myocardial infarction had significant difference among the two groups with the p value was(p=0.001),this strong variance showed that the apical VSR almost always comes with the anterior wall myocardial infarction while the middle VSR mostly comes with the inferior wall myocardial infarction.The affected coronary artery vessel was almost the left anterior descending coronary artery(LAD)in the apical group while the left anterior descending coronary artery(LAD)and the right coronary artery(RCA)were the most common in the middle group with significant difference was(p=0.004).(Table 4).Table 5:A total of 71 patients distributed over class ?,? and ? New York Heart Association classification of heart failure(NYHA).Here we described the relationship between VSR and heart failure based on the clinical classification.There were no patients with class ?,only 3 patients were with class ?,22 patients with class ? and 46 patients with class ?.As it is shown in table 5,age,gender,VSR site and size had no significant difference between each class of heart failure.Mechanical support with Intra Aortic Balloon Pump(IABP)had significant difference between class ? and class ?(n=2,2.82%vs.n=23,32.4%,p= 0.002),while mechanical support with Extra Corporeal Membrane Oxygenation(ECMO)had marginal significant difference(p=0.056).Prodromal angina had also significant difference between class ?,? and ? with the p value was(p=0.041),this strong difference predicted the severity of heart failure.There was significant difference in the affected vessel among the 3 classes of heart failure(p=0.020).Pro-BNP had also strong variance between the 3 classes of heart failure with p value was(p=0.000),which indicated the higher the Pro-BNP value the more severe heart failure.And lastly the LVEF was significantly different among the 3 classes of heart failure(p=0.017),which predicted the lower the LVEF the higher the stage of heart failure.Conclusions1.There is no relationship between the site and size of VSR to the severity of heart failure.2.Presentation with Prodromal angina indicates more severe heart failure and worse prognosis.3.Certain factors(VSR size,LVEF,AMI site and affected coronary artery)can give clue to the site of the ventricular septal rupture(VSR).4.Mechanical support with IABP and ECMO,prodromal angina,affected coronary artery,pro-BNP and LVEF are directly proportionate to the severity of heart failure.5.Diabetes mellitus is a common risk factor of post myocardial infarction ventricular septal rupture. |
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