Septal Infarction Research Articles

Continuous Murmur Caused by a Ventricular Septal Defect Post-Myocardial Infarction: Visual Display With a Handheld Computer

Ventricular septal defects do not typically result in a continuous murmur. The only previously reported case involved a congenital ventricular septal defect. We report a case of an acquired ventricular septal defect following a large anterior myocardial infarction resulting in a continuous murmur. The continous nature was confirmed both with 2D echocardiography and a specially equipped stethoscope in conjuntion with a handheld computer to provide a visual display of the murmur. A proposed mechanism for the continuous murmur was discussed

Early Onset and Progression of Left Ventricular Remodeling After Alcohol Septal Ablation in Hypertrophic Obstructive Cardiomyopathy

Alcohol septal ablation (ASA) reduces left ventricular outflow tract (LVOT) pressure gradient in patients with hypertrophic obstructive cardiomyopathy (HOCM), which leads to left ventricular remodeling. We sought to describe the early to midterm changes and modulating factors of the remodeling process using cardiac MRI (CMR). CMR was performed at baseline and 1 and 6 months after ASA in 29 patients with HOCM (age 52+/-16 years). Contrast-enhanced CMR showed no infarct-related hyperenhancement outside the target septal area. Septal mass decreased from 75+/-23 g at baseline to 68+/-22 and 58+/-19 g (P<0.001) at 1- and 6-month follow-up, respectively. Remote, nonseptal mass decreased from 141+/-41 to 132+/-40 and 111+/-27 g (P<0.001), respectively. Analysis of temporal trends revealed that septal mass reduction was positively associated with contrast-enhanced infarct size and transmural or left-sided septal infarct location at both 1 and 6 months. Remote mass reduction was associated with infarct location at 6 months but not with contrast-enhanced infarct size. By linear regression analysis, percentage remote mass reduction correlated significantly with LVOT gradient reduction at 6-month follow-up (P=0.03). Left ventricular remodeling after ASA occurs early and progresses on midterm follow-up, modulated by CMR infarct size and location. Remote mass reduction is associated with infarct location and correlates with reduction of the LVOT pressure gradient. Thus, myocardial hypertrophy in HOCM is, at least in part, afterload dependent and reversible and is not exclusively caused by the genetic disorder.

Correction of oversensing in a pm-dependent patient upgraded to CRT_CD

Exogenous signals can satisfy ICD TV/FV detection criteria and lead to spurious ICD discharges. Moreover, PM-dependent ICD pts can suffer concomitant prolonged pacing inhibition due to suboptimal reliability of noise reversion mode in ICDs. We report a case of oversensing (OS) in a PM-dependent pt upgraded to CRT-ICD. A pt chronically implanted with a DDD PM because of complete heart block was upgraded to a CRT-ICD device (Contak Renewal 2 H155, Guidant) due to the development of ischemic dilated cardiomyopathy and congestive heart failure. He had his bipolar ventricular PM lead capped and an ICD lead (Endotak Reliance 0148, Guidant) and a CS lead (Easytrak II 4517, Guidant) implanted. At implant the ICD lead was placed as far as possible from the bipolar PM lead,though in vicinity due to a preceding inferior septal infarction. The first postimplant evaluation in ICD clinic, with analysis of real-time and stored intracardiac EGMs, revealed intermittent OS during sinus rhythm, occurring only in the right decubitus position with abducted arm and leading to prolonged inhibition of pacing,with presyncope, and false VF detection, with aborted shocks. OS was demonstrated to result from intermittent physical contact of the distal portions of the active and passive lead in the RV apex. At operative revision, connecting the RV rate-sense port of the ICD to the previously abandoned pacing lead (thus shifting from an integrated bipolar to a true bipolar sensing and reducing the sensing field size) abolished the OS. Subsequent follow-up (22 mos) has been uneventful.field size) abolished the OS. Subsequent follow-up (22 mos) has been uneventful. The effect of a passive endocardial electrode on sensing specificity of an ICD system in a PM-dependent pt can be potentially catastrophic. In our case OS could be overcome simply reducing the size of the sensing field.

Usefulness of myocardial contrast echocardiographic quantification of risk area for predicting postprocedural complications in patients undergoing septal ethanol ablation for obstructive hypertrophic cardiomyopathy

Septal ethanol ablation (SEA) is an alternative to surgical myectomy in patients who have drug-refractory obstructive hypertrophic cardiomyopathy. However, permanent atrioventricular conduction block is seen more frequently with SEA. To determine whether septal infarction risk area (SIRA) predicts outcome in patients who have obstructive hypertrophic cardiomyopathy and are undergoing SEA, we evaluated 51 patients (mean age 60 +/- 16, 53% women) who had a successful SEA at Toronto General Hospital (November 1998 to June 2003). Intracoronary myocardial contrast echocardiography that targeted the contact area between the septum and the anterior mitral leaflet was performed before ethanol injection. End-systolic myocardial contrast echocardiographic frames were color coded for better delineation of contrast borders, and myocardial contrast echocardiographic area was calculated by planimetry. Patients were assigned to 1 of 2 groups by median SIRA value (3.51 cm(2), range 0.4 to 7.8). The 2 groups did not differ significantly in age, medication before SEA, electrocardiographic characteristics, left ventricular function, left atrial diameter, volume of intracoronary ethanol injected, peak creatine kinase after ablation, and baseline and follow-up left ventricular outflow tract gradients at rest. Patients in the large SIRA group had greater hypertrophy and a larger septal artery than did patients in the small SIRA group. In the small SIRA group, 3 patients (11.5%) had pacemaker implantation; in the large SIRA group, 12 patients (48.0%) had complications after SEA (pacemaker in 5 patients, implantable defibrillator in 5 patients, death in 2 patients; p = 0.008). We conclude that patients who have hypertrophic cardiomyopathy with a small, well-localized SIRA benefit similarly from SEA as patients who have a larger SIRA but with significantly fewer serious complications.

Permanent pacing for complete atrioventricular block after nonsurgical (alcohol) septal reduction in patients with obstructive hypertrophic cardiomyopathy

Nonsurgical septal reduction is a newly developed, catheter-based therapeutic option for patients with drug-refractory obstructive hypertrophic cardiomyopathy. A circumscribed septal infarction is generated to reduce the left ventricular outflow tract gradient. The spontaneous regression of complete atrioventricular block after the procedure and the main complication of the intervention are examined, and treatment with permanent pacing is evaluated.

Anaphylaxis to stinging insect with myocardial infarction: A case report

Rationale Anaphylaxis to Hymenoptera venom with associated coronary vasospasm and infarction has been reported rarely. Method Case Report: We present a previously healthy 25 year old black male painter who developed myocardial infarction following alleged sting to the right neck area. Results On the day of admission he was stung while painting at a construction site by a single wasp in the right nuchal region with swelling of both lips within the hour. He was transported to the ER and was unconscious on arrival. He was intubated within 2 hours of presentation and admitted to the ICU after he was given Epi nephrine 0.3 cc 1/1000 subcutaneously and then a second dose down the endotracheal tube. He was given Benadryl 100mg q6h and Decadron 24mg initially then 8mg q8hIVas well as O2 assistance. Labsy) His EKG within 21/2 post admission demonstrated ST/T wave changes consistent with anterior lateral septal wall myocardial infarction with nonspecific ST-T wave changes. He had an ECHO consistent with hypokinesis and anterior/lateral wall septal infarction confirmed by cardiology. His CPK was initially 149u/l (elevated)on the day of admission within 2 hours it was 212u/l with MBSC initially 1.2nanograms/ml on admission then 6.8nanograms/ml within 2hours post admission. Troponin I was undetectable on admission then 11.4 nanograms/ml within 2 hours. He was discharged after 48hours with a normal physical exam. RAST IgE to yellow jacket from one day post admission was 4.41 KU/L (3.5-17.5KU/L antibody level high by QuestDiagnostics Wallingford, CT) class 3, white faced hornet 3.34ku/l (class2), yellow faced hornet 5.48ku/l(class3), paper wasp 2.27ku/l (class2). Conclusion We have presented a case of venom anaphylaxis with myocardial infarction.

Myocardial infarction after percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy: evaluation by contrast-enhanced magnetic resonance imaging

ObjectivesThe aim of this study was to evaluate myocardial infarction induced by percutaneous transluminal septal myocardial ablation (PTSMA) in symptomatic patients with hypertrophic obstructive cardiomyopathy using contrast-enhanced (CE) magnetic resonance imaging (MRI). BackgroundContrast-enhanced MRI delineates the extent of myocardial infarction in coronary artery disease, but its role in ethanol-induced infarction has not been established. MethodsCine and CE MRI were performed before and one month after PTSMA in 24 patients. Size and location of the induced infarction were related to left ventricular (LV) mass reduction, enzyme release, volume of ethanol administered, LV outflow tract gradient reduction, and coronary ablation site. ResultsOne month after PTSMA, regional hyperenhancement was visualized in the basal interventricular septum in all patients. Mean infarction size was 20 ± 9 g, corresponding to 10 ± 5% and 31 ± 16% of total LV and septal mass, respectively. Total LV mass decreased from 219 ± 64 to 205 ± 64 g (p < 0.01), and septal mass from 76 ± 25 to 68 ± 22 g (p < 0.01). Total LV mass reduction exceeded septal mass reduction (p < 0.01). Infarction size correlated with peak creatine phosphokinase-MB (β = 0.67, p < 0.01), volume of ethanol administered (β = 0.47, p = 0.02), total LV and septal mass reduction (β = 0.50, p = 0.02; β = 0.73, p < 0.01), and gradient reduction (β = 0.63, p < 0.01). Seven patients with exclusively right-sided septal infarction had smaller infarction size and less gradient reduction than remaining patients with left-sided or transmural infarction (p < 0.01). In five of these, PTSMA was performed distal in the target artery. ConclusionsContrast-enhanced MRI allowed detailed evaluation of size and location of septal myocardial infarction induced by PTSMA. Infarction size correlated well with clinical indexes of infarct size.

Anteroseptal or apical myocardial infarction: a controversy addressed using delayed enhancement cardiovascular magnetic resonance imaging.

Delayed enhancement MRI (DE-MRI) of the heart has been shown to reliably identify areas of irreversible myocardial damage. We sought to determine if the term anteroseptal MI is appropriate by correlating electrocardiographic, angiographic, cine MRI and DE-MRI findings. Nineteen patients admitted to our hospital with their first acute anterior MI and whose ECG showed new Q waves in leads V1-V4 were studied. All patients underwent cardiac catheterization, cine MRI, and DE-MRI. The mean left ventricular ejection fraction was 53%+/-16%. All 19 patients had evidence of delayed hyperenhancement in one or more myocardial segments (mean number of affected segments 5.5+/-2.1). The mean mass of hyperenhanced myocardium was 14+/-8 grams, or 10%+/-6% of absolute LV mass. Nineteen (100%) and 15 (79%) patients showed evidence of delayed hyperenhancement of the apex and apical anterior segments respectively. Seven (37%) patients showed evidence of mid ventricular anteroseptal hyperenhancement and none had any hyperenhancement of basal anteroseptal segments. High resolution cardiac MRI applied in patients with acute infarction and new Q waves in leads V1-V4 demonstrates the presence of predominantly apical, but not isolated septal or anteroseptal infarction.

Clinical significance of QS complexes in V1 and V2 without other electrocardiographic abnormality.

In the absence of other electrocardiographic (ECG) abnormalities, QS deflections simultaneously in both of the leads V1-V2 may have multiple possible causes. Despite much information in the literature indicating that this is an unlikely pattern for pure septal infarction, such an ECG diagnosis is frequently given. Ninety-nine cases having QS deflections in both leads V1 and V2 but no other ECG abnormality were compared to 99 other patients with entirely normal ECGs, to whom they were matched by age, gender, and the presence or absence of septal Q waves. Retrospective analysis of medical records was performed to determine the nature of any cardiovascular disease in these two groups, and to find a possible explanation for the ECG abnormality. Because of its intermittence in subjects with multiple ECGs, QS deflections in leads V1-V2 appeared most often to be an artifact of precordial lead placement. Prior myocardial infarction, or presence of clinical coronary disease was present in only about 20% of the cases. Neither the intermittence of Q wave in V2 on repeated ECGs nor the absence of septal Q waves was useful in distinguishing between those with and without coronary heart disease. This ECG pattern is a sign of prior myocardial infarction in only a minority of cases, and in the latter, infarction limited to the interventricular septum is exceptional. This ECG finding should be interpreted as a nonspecific QRS abnormality with multiple possible causes. Clinical correlation and repeat tracings with attention to lead placement will help to clarify its significance.

The enigma of optimal treatment for acute ventricular septal rupture

The enigma of optimal treatment for acute ventricular septal rupture

Ablación septal en la miocardiopatía hipertrófica obstructiva

Rev Esp Cardiol 2003;56(12):1231 1231 A 62-year-old patient had symptomatic hypertrophic obstructive cardiomyopathy diagnosed six years ago. Despite medical treatment, dyspnea progressed during follow-up and a two-chamber pacemaker had been implanted one year previously. The reason for the current hospitalization was worsening symptoms (functional class III). The dynamic left ventricular outflow tract gradient was 120 mm Hg by Doppler. Single photon emission computerized tomography (SPECT) myocardial perfusion images showed no perfusion defects (Figure 1A). The patient’s symptoms were refractory to treatment, and percutaneous alcohol septal ablation was recommended. Alcohol injection into a dominant third septal artery branch resulted in septal myocardial infarction. There were no complications and the intraventricular dynamic gradient decreased to 20 mm Hg. Cardiac scintigraphy with 99mTcIM AG E S I N C A R D I O L O G Y

Oclusión con micro-coils de la primera rama septal en el tratamiento de un paciente con miocardiopatía hipertrófica obstructiva

Nonsurgical septal reduction by induced septal infarction is one of the management options in the treatment of patients with hypertrophic obstructive cardiomyopathy. Good immediate and long-term clinical and hemodynamic results have been reported with this technique for occlusion of the first septal branch of the anterior descending coronary artery followed by ethanol infusion. This is the first report of a case in which nonsurgical septal reduction with microcoils has been attempted.

Atrial septal defect and myocardial infarct

The etiology for an acute myocardial infarction with normal coronary arteriography should rule in and rule out the presence of an atrial septal defect. Acute increases in left to right shunting with an atrial septal defect may lead to episodes of myocardial necrosis and right ventricular dysfunction. This case report describes such a scenario.

Role of controlled septal infarct in hypertrophic obstructive cardiomyopathy.

Hypertrophic obstructive cardiomyopathy is a complex and challenging disease. Medical therapy, surgical therapy, and pacing therapy have been used with some success over the years. Nonsurgical septal reduction therapy, also called alcohol septal ablation, has been used recently as a percutaneous catheter-based intervention to improve left ventricular outflow tract obstruction and thereby improve symptoms. The reported results of this procedure have shown impressive reductions in gradient and improvement in symptoms at relatively low risk. The most common complication of the procedure, development of complete heart block requiring a permanent pacemaker, has improved in recent studies with refinements of the procedural technique. Nonsurgical septal reduction therapy has been shown to improve diastolic function, decrease left ventricular hypertrophy and mass, and cause changes at the cellular and molecular level that improve myocardial function. Reported results at 1 year follow-up continue to show benefit, and long-term studies are ongoing.

C-reactive protein elevation following chemically induced septal infarction in humans without coronary atherosclerosis

C-reactive protein elevation following chemically induced septal infarction in humans without coronary atherosclerosis

Ein-Jahresverlauf nach echokardiographisch geführter perkutaner Septumablation bei hypertropher obstruktiver Kardiomyopathie

Percutaneous transluminal septal myocardial ablation by alcohol-induced septal branch occlusion was introduced as a new treatment option in symptomatic patients with hypertrophic obstructive cardiomyopathy. Echocardiographic monitoring of the procedure resulted in improvement of acute results. In this study we analyzed the follow-up after echocardiographic guided septal ablation. 100 consecutive symptomatic patients (50 men; age 52.7 +/- 15.7 years; NYHA class 2.8 +/- 0.6) underwent percutaneous septal ablation with echocardiographic monitoring. All patients had clinical and non-invasive 3-months and 1 year follow-up. Acute reduction of the left ventricular outflow tract gradient was achieved in 99 patients from 76 +/- 37 to 19 +/- 21 mm Hg at rest, from 104 +/- 34 to 43 +/- 31 mm Hg during Valsalva maneuver, and from 146 +/- 45 to 59 +/- 42 mm Hg post extrasystole (p < 0.0001, each). Mean CK rise was 570 +/- 236 U/l. One patient died at day 2 due to fulminant pulmonary embolism following deep venous thrombosis, and 8 patients required a permanent DDD-pacemaker due to postinterventional complete heart block. During follow-up no further patient died. All living 99 patients showed clinical improvement to NYHA-class 1.4 +/- 0.6 after 3 months and 1.5 +/- 0.6 after 1 year (p < 0.0001, each). Non-invasive follow-up studies observed ongoing outflow tract gradient reduction, decrease of septal and left ventricular posterior wall thickness, and improvement of exercise capacity and time. Percutaneous septal ablation is an effective treatment of symptomatic patients with hypertrophic obstructive cardiomyopathy. During one-year follow-up remodeling after induced therapeutic septal infarction resulted in improvement of acute gradient reduction with ongoing symptomatic and objective improvement and without significant complications and side-effects.

Non-surgical myocardial reduction for patients with hypertrophic obstructive cardiomyopathy

Until 1994 surgical myotomy-myectomy was the most effective symptomatic treatment for patients with symptoms of hypertrophic cardiomyopathy and dynamic left ventricular outflow tract obstruction refractory to pacing and drug treatment. Similar functional results can now be achieved by the creation of an alcohol-induced septal infarction using a catheter technique. This therapeutic myocardial necrosis results in widening of the left ventricular outflow tract with consequent gradient reduction, followed by clinical and objective improvement, as well as further gradient reduction as a result of left ventricular remodelling.

Pressure-guided nonsurgical myocardial reduction induced by small septal infarctions in hypertrophic obstructive cardiomyopathy

OBJECTIVESWe sought to assess the safety and efficacy of pressure-guided nonsurgical myocardial reduction (NSMR) with the induction of small septal infarctions in patients with hypertrophic obstructive cardiomyopathy (HOCM).BACKGROUNDNonsurgical myocardial reduction has been shown to decrease left ventricular outflow tract (LVOT) obstruction and to improve symptoms in patients with HOCM. Infarct sizes differ considerably among studies published so far.METHODSIn 50 patients, the LVOT gradient was invasively determined at the time of the intervention, four to six months (n = 49) and 12 to18 months (n = 25) after NSMR. New York Heart Association functional class and quality of life were assessed by using a standard questionnaire. Exercise capacity was tested by spiro-ergometry. Left ventricular (LV) mass was determined by electron beam computed tomography.RESULTSSmall septal infarctions (mean creatine kinase value 413 ± 193 U/l) resulted in a sustained decrease in LVOT gradients, from 80 ± 33 to 18 ± 17 mm Hg after four to six months (p < 0.001, n = 49) and to 17 ± 15 mm Hg (p < 0.001, n = 25) after 12 to 18 months. Nonsurgical myocardial reduction was followed by a decrease in LV hypertrophy, which was associated with a sustained increase in exercise capacity, as well as improvement in quality of life.CONCLUSIONSPressure-guided NSMR inducing small septal infarctions was sufficient to result in a sustained decrease in LVOT obstruction and to improve symptoms. The incidence of complications, such as complete heart block with necessary permanent pacemaker implantation (<10%), seems to be diminished by minimizing the infarct size.

Percutaneous transluminal septal myocardial ablation: A new catheter-based therapy for patients with hypertrophic obstructive cardiomyopathy

Hypertrophic obstructive cardiomyopathy is a complex disorder with serious clinical implications. Percutaneous transluminal septal myocardial ablation is a promising new addition to existing therapies for this condition. It is a catheter-based approach that involves instilling alcohol into the septal branches of the left anterior descending artery to induce a ‘controlled’ septal myocardial infarct. The result is a decrease in thickness of the hypertrophied interventricular septum and a reduction of the left ventricular outflow tract gradient. To date, the results from several series have been promising, with improvements in haemodynamic and clinical parameters without prohibitive complication rates. In this article, the indications, technique and outcomes of this procedure are reviewed.

Acute Electrocardiographic Changes After Pneumonectomy*

Postpneumonectomy electrocardiographic (ECG) changes have not been well-defined. We reviewed the clinical data and the preoperative and postpneumonectomy ECGs of 15 patients who had pneumonectomy. All postpneumonectomy ECGs showed a higher heart rate and two (13%) showed diffuse ST elevation. Four patients (27%) had transient atrial arrhythmias. Five patients (33%) had some ECG findings of acute cor pulmonale. A leftward shift of the QRS axis occurred after left pneumonectomy. The precordial transitional zone shifted counterclockwise after right pneumonectomy. Except for one case of septal myocardial infarction, postpneumonectomy ECG changes appeared to result from the pneumonectomy and not from cardiopulmonary disease. Recognition of expected postpneumonectomy ECG findings will help avoid confusing these changes with acute cardiac and pulmonary events, which should reduce patient morbidity and costs.