Reciprocal ST Depression Research Articles

Kounis Syndrome: A Stinging Case of ST-Elevation Myocardial Infarction

Kounis syndrome is not a rare but an infrequently diagnosed non-thrombogenic cause of angina or myocardial infarction triggered by the release of inflammatory mediators following an allergic or anaphylactic reaction. This so-called "allergic angina" is seen in the setting of anaphylactic reactions and is believed to be due to mast cell release causing coronary vasospasm. The treatment of such cases is often with epinephrine, which has also been described in the literature as another rare cause of coronary vasospasm. We present a case of Kounis syndrome seen in a 46 year-old male who suffered two bee stings while landscaping in his yard. He developed an anaphylactic reaction and was promptly treated with IM epinephrine injection by paramedics at arrival and developed marked ST elevations on EKG in the inferior leads with reciprocal ST depressions in the anterior leads. His troponin peaked at 13 ng/mL and tryptase level was 15 ng/mL (normal <10 ng/mL). Coronary catheterisation showed non-diseased coronary arteries and a normal ejection fraction without evidence of vasospasm. He was afterwards treated with an epinephrine drip for distributive shock. Interestingly this syndrome was not provoked when re-challenged with this therapy, suggestive of an allergic reaction rather than epinephrine as the aetiology of his presumed vasospasm. This patient's ST segment elevation and troponin elevation was due to Kounis syndrome. Awareness that anaphylactic reactions can lead to Kounis syndrome can lead to prompt appropriate treatment for this life threatening condition.

Differentiating between comatose patients resuscitated from acute coronary syndrome-associated and subarachnoid hemorrhage-associated out-of-hospital cardiac arrest

BackgroundUpon initial evaluation in the emergency department (ED), it is often difficult to differentiate between comatose patients resuscitated following acute coronary syndrome (ACS)-associated and subarachnoid hemorrhage (SAH)-associated out-of-hospital cardiac arrest (OHCA). We assessed the clinical differences between resuscitated comatose ACS-OHCA and SAH-OHCA patients during initial evaluation in the ED. MethodsData of 1259 consecutive OHCA patients were analyzed retrospectively. Of these, 23 resuscitated comatose ACS-OHCA patients and 20 resuscitated comatose SAH-OHCA patients were included in the final analysis. Clinical data obtained during initial evaluation in the ED were compared between groups. ResultsPulseless electrical activity (PEA) or asystole as the initial cardiac rhythm, female gender, and preserved left ventricular ejection fraction (≥50%) on the echocardiogram were significantly more common in the SAH-OHCA group (p<0.05 each). Although ST-T abnormalities suggesting myocardial damage (ST elevation and/or ST depression) were noted in most patients in both groups via 12-lead electrocardiogram (95%, ACS-OHCA group; 85%, SAH-OHCA group, p=0.50), reciprocal ST depression was significantly more often absent in the SAH-OHCA group (p=0.025). Initial PEA/asystole and presence of 1 other factor was sufficient to differentiate SAH-OHCA patients from ACS-OHCA patients (100% sensitivity, 91% specificity, 95% accuracy). ConclusionsInitial ED evaluation is sufficient to differentiate between comatose ACS-OHCA and SAH-OHCA patients prior to further diagnostic work-up (e.g. emergent coronary angiography and head computed tomography).

Electricity, Heart and ST-Segment Elevation: A Closer Look

Dear Editor,We read with great interest the article by Uyanik et al., entitled “Delayed ST-Segment Elevation Due to Electrical Injury Mimicking Acute Myocardial Infarction,” which was published recently in this journal. This case report was mentioning a young patient admitted with late-onset chest pain and ST-segment elevation following ele-ctrical injury (1). Although the case was presented precisely, some points merit further highlighting.Abnormal electrocardiography (ECG) may be found in approxi-mately 31% of patients following an electric shock (2). Non-specific ST-segment changes and sinus tachycardia are the most commonly reported ECG findings; QT prolongation, bundle branch block, atrial and ventricular fibrillation, and atrial and ventricular premature con-tractions are also detected. As referred to in this case report, ST-seg-ment elevation with or without myocardial involvement may follow electrical injury.In a clinical setting, ST-segment elevation on ECG may be related with many conditions, such as myocardial infarction, early repolariza -tion, electrolyte imbalance, and pericarditis. In this case, myocardial infarction may easily be excluded, since cardiac biomarkers are nor-mal and ST elevation is not consistent with myocardial infarction. In this case, ECG shows diffuse and concave ST elevation (elevated at the J point) with the exception of V1 and aVR. In acute myocardial infarction, ST elevation is also accompanied by reciprocal ST depres-sions. In the case of early repolarization, ST elevation is most often present in the mid- to lateral chest leads (V3-V6), and the majority of subjects with early repolarization has no ST deviations in the limb leads. So, early repolarization would be excluded in this patient, who has pronounced ST elevation on D2, D3, and aVF.Zeana describes a 65-year-old electrocuted subject who experi-enced precordial pain, serous enzymes of negative myocardial necro -sis, and ST elevation during 2 weeks of hospitalization (3). These fin-dings suggest the possibility of widespread pericardial involvement. In the case presented by Uyanik et al., pericardial involvement seems to be the most possible cause of ST changes in the admission ECG. This ECG shows us sinus bradycardia with diffuse concave ST elevati-on except for V1 and aVR. ST depression in V1 and aVR is also a typical finding for acute pericarditis. Late-onset chest pain also supports this condition. However, addition of a follow-up ECG of the patient to the report would be more valuable for confirmation of this diagnosis. In our opinion, pericarditis deserves discussion as a possible diagnosis in the aforementioned case.

New Electrocardiographic Criteria to Differentiate Acute Pericarditis and Myocardial Infarction: Rossello X, Wiegerinck RF, Alguiersuari J, et al. Am J Med 2014;127:233–9.

Accurately diagnosing ST-segment elevation myocardial infarctions (STEMIs) in the emergency department can prove to be a challenging task, and misdiagnosis can lead to unnecessary coronary angiography. This article from four tertiary hospitals in Spain sought to improve the distinction between pericarditis and STEMI by examining the duration of the QRS complex and QT interval. The authors hypothesized that the QRS interval would be prolonged in acute MI due to slowed propagation of the local activation front by transmural ischemia; the QT interval was expected to be shortened in the acute period. They performed a multi-centric case-control study examining 150 patients with acute chest pain associated with ST elevation: 71 who presented with STEMIs and 79 who had acute pericarditis. Admission electrocardiograms (ECGs) were manually analyzed for deviation of the PR segment from baseline, ST-segment deviation from the J-point, QRS duration, and QT interval. Each ECG was analyzed using one of three models: Model A included the duration of the QRS complex and QT interval; Model B utilized the classic ECG criteria of PR deviation and J-point level in aVR, as well as the number of leads with ST-segment elevation, ST-segment depression, and PR depression; and Model C tested all of the above variables. Receiver operating characteristic curves (ROCs) were constructed for each model, and the ROCs were compared using the DeLong method. Overall, patients with acute pericarditis were younger with fewer cardiac risk factors. Additionally, these patients showed greater upright PR deviation and deeper J-point in aVR, as well as a higher number of ECG leads with ST elevation and PR depression and a lower number of leads with reciprocal ST depression compared to STEMI ECGs. In patients with pericarditis, the QRS and QT intervals were the same in leads with and without ST elevation, whereas patients diagnosed with STEMIs showed a longer duration of the QRS complex and shorter QT interval length in leads with ST elevation compared to isoelectric leads. Comparison of the aforementioned models showed improvement in the ROC when QRS and QT interval duration were included in the analysis, with the ROC for model A being 0.807, model B 0.863, and model C 0.914. This study demonstrates that factoring the QRS duration and QT interval in your analysis of an ECG can help the clinician identify pericarditis and acute STEMI. The authors note that the study was limited by a lack of randomization, and that the ECG findings significantly influenced the ultimate diagnosis for patients at discharge.

ST-Segment Elevation Myocardial Infarction vs. Hypothermia-Induced Electrocardiographic Changes: A Case Report and Brief Review of the Literature

BackgroundDiagnosed ST-segment elevation myocardial infarction (STEMI) usually prompts rapid cardiac catheterization response. ObjectiveOur aim was to raise awareness that hypothermia can cause electrocardiographic (ECG) changes that mimic STEMI. Case ReportEmergency Medical Services (EMS) was called for altered mental status and lethargy in a 47-year-old man with a medical history of paraplegia. His history included hepatitis C, hypertension, seizures, anxiety, and recent pneumonia treated with i.v. antibiotics. When brought in by EMS, the patient was responsive only to painful stimuli. His blood glucose was 89 mg/dL; blood pressure was 80/50 mm Hg, and ECG showed ST elevations diffusely. His vital signs in the emergency department were heart rate 53 beats/min, blood pressure 134/79 mm Hg, respiratory rate 14 breaths/min, pulse oximetry of 100%, and a rectal temperature of 32.7°C (91°F). A second ECG showed diffuse ST elevation, sinus bradycardia with a rate of 56 beats/min, and a first-degree atrioventricular block. J waves were noted in V3−V6, I and II. There were no reciprocal changes or ST depressions. A bedside ultrasound showed no pericardial effusion. The patient underwent cardiac catheterization, which showed no coronary artery disease and a normal ejection fraction. Later, hypercapneic respiratory failure with bilateral pneumonia developed and was intubated. His ECG the following day, once he was rewarmed, showed complete resolution of ST elevation and almost complete resolution of J waves. ConclusionObtaining a complete set of vital signs is key to making a correct diagnosis. Hypothermia should be considered in the differential diagnosis of ST elevation.

Regional pericarditis or an alternate diagnosis?

We read the paper by Alhammouri and Omar published in a recent issue of the Case Reports in Medicine [1]. The authors have described a case of what appeared to be a case of localized pericarditis; however, we wonder if alternate diagnosis was considered in the differential diagnosis. The initial ECG illustration shows ST-elevation localized to the inferior leads with reciprocal ST-depressions in V1–V3 which is usually quite unusual for acute pericarditis [2]. Spodick's sign has traditionally been defined in prior investigations by the senior author as an electrocardiographic clue to help differentiating between acute pericarditis and acute myocardial infarction; however, to best of our knowledge, this is usually valid in absence of reciprocal ST-depressions [2–6]. The pathophysiogenesis of the Spodick's sign is likely related to the diastolic injury current. During diastole, the injured subepicardial zone remains partly polarized (probably due to reduced resting transmembrane potential), as in systole. Thus, there is a potential difference between it and the completely polarized remaining myocardial mass, producing a diastolic injury current oppositely oriented to the systolic injury current that shifts electrical diastole, the TQ interval. This interval corresponds to the ECG baseline (TP) and cannot be detected by the clinical ECG so that it appears as a J (ST) shift in the opposite direction [2]. Similarly, authors have used the term “reverse Spodick's sign” which merely simulates reciprocal ST-depressions; however, in our opinion, it needs a validation in large controlled investigations if indeed it is associated with acute localized pericarditis. Cardiac magnetic resonance imaging would have been helpful in this case for diagnostic confirmation [7]. Also, the authors have mentioned normal right coronary and left anterior descending arteries. What about left circumflex artery: was that also normal? Notably, the second ECG obtained after a few hours shows complete normalization of prior ST-T changes without any use of anti-inflammatory therapies (NSAID's or Colchicine) and, in fact, did not demonstrate dynamic ECG changes of four-stage pericarditis [2, 3, 7]. This makes us wonder if other potential explanation such as transient coronary vasospasm may serve as an explanation for the noted clinical and ECG changes on the initial presentation.

Reciprocal ECG change in reperfused ST-elevation myocardial infarction is associated with myocardial salvage and area at risk assessed by cardiovascular magnetic resonance

ObjectiveST-elevation acute myocardial infarction (STEMI) is frequently associated with reciprocal ST depression in contralateral ECG leads. The relevance of these changes is debated. This study examined whether reciprocal ECG changes...

093 RECIPROCAL ECG CHANGE IN ST-ELEVATION MYOCARDIAL INFARCTION IS ASSOCIATED WITH AREA AT RISK AND MYOCARDIAL SALVAGE FOLLOWING REVASCULARIZATION

<h3>Background</h3> ST elevation acute myocardial infarction (STEMI) is frequently associated with reciprocal ST depression in the contralateral ECG leads. The ECG remains a primary diagnostic factor in the hyperacute treatment of myocardial infarction. There has been longstanding debate over the relevance of reciprocal ECG changes in STEMI. CMR can retrospectively determine myocardial area at risk (AAR), namely, the area of myocardium that is susceptible to infarction prior to opening the infarct-related artery. T2-weighted (T2w) imaging can be combined with measures of infarction by late gadolinium enhanced (LGE) imaging to derive myocardial salvage, a measure with established prognostic relevance. We hypothesised that reciprocal ECG change reflects larger AAR as defined by CMR. <h3>Methods</h3> Patients after primary percutaneous coronary intervention for first STEMI underwent CMR at 1.5 T within 3 days of reperfusion. Presenting ECGs were assessed for presence or absence of reciprocal change, defined as ≥1 mm ST depression in ≥2 inferior leads for anterior STEMI, or ≥2 anterior leads for inferior STEMI. Patients with posterior ECG changes were excluded from analysis. Infarcted tissue was defined as hyperenhancement ≥2 SDs above remote myocardium on LGE imaging. AAR was defined on T2w images, defined as the mass of myocardium with signal intensity ≥2 SD above remote, normalised to LV myocardial mass (figure&nbsp;1). Myocardial salvage was calculated as (AAR mass—infarct mass), and myocardial salvage index as (myocardial salvage/AAR mass). <h3>Results</h3> Thirty-five patients had ECGs and images suitable for analysis. There were no significant differences in patient demographics (table&nbsp;1). Patients with reciprocal ECG changes had significantly higher AAR than those without (42.3% vs 23.6%, p&lt;0.001), myocardial salvage (17 g vs 2 g, p&lt;0.001) and myocardial salvage index (40% vs 7%, p&lt;0.001). Infarct size was not significantly different between patients with and without reciprocal ECG changes (25.6 g vs 27.4 g, p=0.8), nor was ejection fraction (43% vs 45%, p=0.5) or LV end diastolic volume (173 ml vs 174 ml, p=0.9). <h3>Conclusions</h3> Patients with STEMI presenting with reciprocal ECG changes have significantly larger AAR, and significantly higher myocardial salvage and salvage index than those without. Reciprocal ECG changes may be a marker of larger volumes of myocardium at risk, and may also denote patients with larger potential for salvage with revascularization. There was no relationship to infarct size, presumably as other factors, such as time to revascularization and TIMI flow post-procedure will influence the degree of myocardium infarcted. Data are shown as mean±SEM or n (%). There were no significant differences between the groups (p≥0.1 for all).

Reciprocal ECG change in ST-elevation myocardial infarction is associated with area at risk and myocardial salvage following revascularization

Background ST elevation acute myocardial infarction (STEMI) is frequently associated with reciprocal ST depression in the contralateral ECG leads. The ECG remains a primary diagnostic factor in the hyperacute treatment of AMI. There has been longstanding debate over the relevance of reciprocal ECG changes in AMI. CMR can retrospectively determine myocardial area at risk (AAR), namely, the area of myocardium that is susceptible to infarction prior to opening the infarct-related artery. T2-weighted (T2w) imaging can be combined with measures of infarction by late gadolinium enhanced (LGE) imaging to derive myocardial salvage, a measure with established prognostic relevance. We hypothesised that reciprocal ECG change reflects larger AAR as defined by CMR. Methods Patients after primary percutaneous coronary intervention for first STEMI underwent CMR at 1.5T within 3 days of reperfusion. Presenting ECGs were assessed for presence or absence of reciprocal change, defined as ≥1mm ST depression in ≥2 inferior leads for anterior STEMI, or ≥2 anterior leads for inferior STEMI. Patients with posterior ECG changes were excluded from analysis. Infarcted tissue was defined as hyperenhancement ≥2 standard deviations (SD) above remote myocardium on LGE imaging. AAR was defined on T2w images, defined as the mass of myocardium with signal intensity ≥2 SD above remote, normalized to LV myocardial mass. Myocardial salvage was calculated as (AAR mass infarct mass), and myocardial salvage index as (myocardial salvage / AAR mass). Results Thirty-five patients had ECGs and images suitable for analysis. There were no significant differences in patient demographics (Table 1). Patients with reciprocal ECG changes had significantly higher AAR than those without (42.3% vs. 23.6%, p<0.001), myocardial salvage (17g vs 2g, p<0.001) and myocardial salvage index (40% vs. 7%, p<0.001). Infarct size was not significantly different between patients with and without reciprocal ECG changes (25.6g vs. 27.4g, p=0.8), nor was ejection fraction (43% vs. 45%, p=0.5) or LV end diastolic volume (173ml vs. 174ml, p=0.9). Conclusions Patients with STEMI presenting with reciprocal ECG changes have significantly larger AAR, and significantly higher myocardial salvage and salvage index than those without. Reciprocal ECG changes may be a marker of larger volumes of myocardium at risk, and may also denote patients with larger potential for salvage with revascularization. There was no relationship to infarct size, presumably as other factors, such as time to revascularization and TIMI flow post-procedure will influence the degree of myocardium infarcted.

Allergic myocardial infarction

Allergic myocardial infarction

False Positive ST-Segment Elevation Myocardial Infarction

False Positive ST-Segment Elevation Myocardial Infarction

Reciprocal ST segment changes in acute inferior myocardial infarction: Clinical, hemodynamic and angiographic implications

To investigate the clinical significance of reciprocal ST segment depression on the presenting electrocardiogram in patients with acute inferior myocardial infarction. Design and setting: A prospective, randomized, controlled single center study done in the critical care department, Cairo university Hospital. Forty consecutive patients with acute inferior myocardial infarction were enrolled in this study divided into two groups, 20 patients with reciprocal ST depression (group 1) and 20 patients without such depression (group 2). Interventions: All patients were investigated with serial ECG, cardiac biomarkers, echocardiography and coronary angiography. There was no significant difference in the proportion of coronary disease risk factors in patients in group 1, versus those in group 2. Patients in group 1 had significant higher degree ST elevation (in inf. Leads) than patients in group 2, higher levels of peak total CPK and CKMB was also seen. In addition patients in group 1 developed complication more frequently than those in group 2. Although no statistically significant difference between the two groups was seen as regard the ejection fraction sought by echocardiography, it did show a higher incidence of mitral regurge in group 1 [14 (70%)] versus 6 (30%) in group 2 with P value of 0.01. In group 1 left anterior descending artery lesions was significantly more frequent than in group 2 with P value < 0.001, also multivessel disease was significantly more frequent in group 1. The significance of reciprocal ST depression on the electrocardiogram during the course of inferior MI remains uncertain, opinion is divided as to whether it is a benign electrical phenomenon or a sign of a greater myocardial necrosis and more frequent left coronary artery disease, from our study we support the latter opinion. This simple ECG finding may be used to differentiate high risk patients for a more aggressive approach.

PREDICTORS OF FAILED THROMBOLYSIS IN ACUTE MYOCARDIAL INFARCTION

objectives: Acute myocardial infarction(AMI) is becoming increasingly important problem in developing countries, and thrombolysis is the main modality of treatment here. About 25-50% of patients fail to achieve successful reperfusion and these patients have poor prognosis. Since alternative modes of reperfusion are available, it is important to identify them. This study was aimed at defining the extent of failed thrombolysis and identifying its demographic and clinical predictorsMethods: 50 cases of thrombolysed AMI patients were studied. Failed thrombolysis considered if there is 0.05), percentage of females was 25% v/s 16.7%(P>0.05), mean time for resolution of chest pain was 3.55±1.1 hrs v/s. 1.98±0.93 hrs (P 0.05), inferior wall MI was 30% v/s 46% (P>0.05) in failed and successful group respectivly. Interpretation and conclusion.Late presentation is an important risk factor for failed thrombolysis in AMI. Persistence of chest pain and non-resolution of reciprocal ST depression are significantly associated with failed thrombolysis.

Basilar artery occlusion after acute myocardial infarction

A 53-year old patient was admitted to the emergency department with acute chest pain, nausea and dyspnea. He had several vascular risk factors such as cigarette smoking, overweight and hypercholesteremia. 12-lead ECG showed ST elevation in the inferior and lateral leads and reciprocal ST depression in the anteroseptal leads indicating acute inferoposterior myocardial infarction. Coronary angiography demonstrated thrombotic occlusion of the proximal left circumflex artery. The occlusion was successfully recanalized by thrombus aspiration and stabilized with an everolimus-eluting stent (Fig. 1). The ventriculography suggested a mild impairment of the left ventricular ejection fraction with profound inferior hypokinesia. Antithrombotic therapy with salicylic acid, clopidogrel and lowmolecular weight heparin was started. Twelve hours later the patient complained of acute headache, vertigo and bilateral hearing loss and minutes later his consciousness decreased. The neurological assessment showed left sided facial palsy, Horner's syndrome and skewdeviation. A detailed sensorimotor assessment of the extremities was impossible due to coma. Intracerebral bleeding was ruled out by computed tomography. The neurologic findings suggested an acute brainstem lesion. The initial NIHSS Score (National Institute of Health Stroke Scale) was assessed to 15 points. The

Basilar artery occlusion after acute myocardial infarction

A 53-year old patient was admitted to the emergency department with acute chest pain, nausea and dyspnea. He had several vascular risk factors such as cigarette smoking, overweight and hypercholesteremia. 12-lead ECG showed ST elevation in the inferior and lateral leads and reciprocal ST depression in the anteroseptal leads indicating acute inferoposterior myocardial infarction. Coronary angiography demonstrated thrombotic occlusion of the proximal left circumflex artery. The occlusion was successfully recanalized by thrombus aspiration and stabilized with an everolimus-eluting stent (Fig. 1). The ventriculography suggested a mild impairment of the left ventricular ejection fraction with profound inferior hypokinesia. Antithrombotic therapy with salicylic acid, clopidogrel and lowmolecular weight heparin was started. Twelve hours later the patient complained of acute headache, vertigo and bilateral hearing loss and minutes later his consciousness decreased. The neurological assessment showed left sided facial palsy, Horner's syndrome and skewdeviation. A detailed sensorimotor assessment of the extremities was impossible due to coma. Intracerebral bleeding was ruled out by computed tomography. The neurologic findings suggested an acute brainstem lesion. The initial NIHSS Score (National Institute of Health Stroke Scale) was assessed to 15 points. The

Rupture of the Posteromedial Papillary Muscle Leading to Partial Flail of the Anterior Mitral Leaflet

HomeCirculationVol. 123, No. 9Rupture of the Posteromedial Papillary Muscle Leading to Partial Flail of the Anterior Mitral Leaflet Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessResearch ArticlePDF/EPUBRupture of the Posteromedial Papillary Muscle Leading to Partial Flail of the Anterior Mitral Leaflet Michael G. Fradley and Michael H. Picard Michael G. FradleyMichael G. Fradley From the Department of Medicine, Division of Cardiology, Massachusetts General Hospital, Boston. Search for more papers by this author and Michael H. PicardMichael H. Picard From the Department of Medicine, Division of Cardiology, Massachusetts General Hospital, Boston. Search for more papers by this author Originally published8 Mar 2011https://doi.org/10.1161/CIRCULATIONAHA.110.984724Circulation. 2011;123:1044–1045An 86-year-old woman with a history of hypertension presented with acute onset of chest pain and evidence of shock (hypotension and tachycardia). For the preceding 2 weeks, she had been experiencing intermittent nausea and vomiting; proton pump inhibitors did not improve her symptoms. The ECG showed ST elevations in the inferior leads and ST depressions in leads V1 and V2, with reciprocal ST depressions in leads I and aVL, suggesting an acute inferoposterior infarction (Figure 1). Physical examination also revealed a new 2/6 holosystolic murmur at the apex and significant bilateral rales. She was taken emergently to the cardiac catheterization laboratory, where 100% thrombotic occlusion of the middle right coronary artery was revealed (Figure 2A). A left ventriculogram revealed severe (4+) mitral regurgitation with a normal-sized left atrium (Figure 2B). An intra-aortic balloon pump was placed, and she was transferred to the cardiac intensive care unit. A transthoracic echocardiogram revealed normal right and left ventricular size and function, with evidence of inferior and posterior wall hypokinesis. The estimated pulmonary artery systolic pressure was significantly elevated at 77 mm Hg. Most important, however, the echocardiogram confirmed both severe mitral regurgitation with rupture of the posteromedial papillary muscle and partial flail of the anterior mitral leaflet (Figure 3A through D; Movies I through III in the online-only Data Supplement). Unfortunately the patient's clinical status continued to worsen. She was deemed extremely high risk for surgery, and her healthcare proxy confirmed her do-not-resuscitate/do-not-intubate status. She expired several hours later despite maximal hemodynamic support.Download figureDownload PowerPointFigure 1. Twelve-lead surface ECG showing ST elevations in leads II, III, and aVF and ST depressions in leads V1, V2, I, and aVL, suggesting acute inferoposterior myocardial infarction.Download figureDownload PowerPointFigure 2. A, Right coronary artery angiogram demonstrating midvessel occlusion (arrow). B, Left ventriculogram, right anterior oblique view, demonstrating severe mitral regurgitation. LA indicates left atrium; LV, left ventricle; and Ao, aorta.Download figureDownload PowerPointFigure 3. Transthoracic echocardiogram images in the parasternal long-axis (A and B) and apical 2-chamber (C) views demonstrating the ruptured posteromedial papillary muscle (arrow) and partial flail/prolapse of the anterior mitral leaflet (arrowhead). D, Transthoracic echocardiogram, parasternal long-axis view with color Doppler, demonstrating severe mitral regurgitation. LA indicates left atrium; LV, left ventricle; and RV, right ventricle.Acute mitral regurgitation caused by papillary muscle rupture is a rare but life-threatening complication of myocardial infarction. Patients typically present with an inferior infarction with the right coronary artery as the culprit. They also tend to be older and have a preserved ejection fraction. Rupture typically occurs within 5 days of the infarct.1 It is postulated that the preserved contractility exerts increased stress on an already compromised papillary muscle, eventually leading to rupture.2This case highlights the importance of understanding mitral valve anatomy. The valve itself comprises an anterior and a posterior leaflet. Valvular competence is maintained by the 2 papillary muscles (anterolateral and posteromedial) that are attached to the leaflets via the chordae tendinae. Typically, the anterolateral muscle is a single large structure, whereas the posteromedial muscle can have 1 to 3 heads.3 The 2 papillary muscles send chordae tendinae to both leaflets of the mitral valve; as a result, either leaflet can be affected by rupture of either papillary muscle. Blood supply to the anterolateral muscle is supplied by both the left anterior descending and circumflex arteries, whereas the posteromedial muscle is supplied only by the right coronary artery. Rupture of the posteromedial muscle is more common because of its single blood supply.4Echocardiography is useful in the diagnosis of papillary muscle rupture with a sensitivity of 65% to 85%.4 Although it may be easy to identify prolapse or flail of the dysfunctional leaflet and the direction of the regurgitant jet on echocardiography, these findings do not reliably predict the affected papillary muscle, and direct visualization of the rupture is necessary for definitive diagnosis.DisclosuresNone.FootnotesThe online-only Data Supplement is available with this article at http://circ.ahajournals.org/cgi/content/full/123/9/1044/DC1.Correspondence to Michael Fradley, MD, Massachusetts General Hospital, Boston, MA 02114. Email [email protected]org

Embolisation of a non-culprit coronary artery complicating thrombus aspiration in acute myocardial infarction: The “drag and drop” effect of the thrombus aspiration catheter

A fifty seven year-old male presented with acute central chest pain waking him up from sleep. He reported exertional chest pain in the weeks preceding and had a background of hypertension, hypercholesterolemia and was an ex-smoker. His examination on arrival was unremarkable and remained haemodynamically stable. His ECG on arrival showed inferior-lateral ST elevation with reciprocal ST depression in anterior leads and Q waves in leads III, aVF. He was treated for aspirin, clopidogrel, low molecular weight heparin and nitrates. He proceeded to have an urgent coronary angiogram with a view to primary angioplasty for acute ST-elevation myocardial infarction.

On the blindside of the ECG lies critical coronary disease

A 46-year-old man presented to the mobile coronary care unit following acute central chest pain radiating to his left arm at rest. He was seen out of hospital 7 min from onset of symptoms. He had suffered from inferior-territory ST-elevation myocardial infarction (STEMI) 3 years previously, with percutaneous intervention (PCI) to the right coronary artery (RCA). His only risk factor was a family history of ischaemic heart disease (his mother aged 42 years had coronary artery bypass grafting). At first medical contact, he was haemodynamically stable [blood pressure (BP) 112/76 mmHg] and clinical examination revealed no abnormality. Twelve-lead electrocardiogram (ECG) had 1 mm STE in aVR, ST-depression in I, II, aVF, V3–V6 and T-wave inversion in aVL (Figure 1a). Concomitant body surface potential mapping (BSPM), utilizing 80 surface electrodes, revealed high right anterior and posterior STEMIs with reciprocal lateral ST-depression (Figure 1b). …

Importance of Reciprocal ST Segment Depression in the Extensive Coronary Artery Disease

Aim: We investigated the relationship between the severity of reciprocal ST depression and the extent of coronary artery disease in patients with inferior myocardial infarction. Method: Ninety-five consecutive patients (52 women 43 men, with a mean age of 54±5 years) who had acute inferior myocardial infarction were included in the study. Reciprocal changes in the ST segment were defined as ST depression of >1 mm in at least two out of four of the precordial leads V1–V4. All the patients had undergone coronary angiography within seven days of admission. The extension of coronary artery disease which was measured by Gensini and Reardon scores, was compared with the reciprocal changes on ECG recorded at the time of admission. Result: There was a significant correlation between reciprocal ST depression and disease extension (r=0.68 for Gensini score, r= 0.88 for Reardon score, p<0.05 for both). Conclusion: The presence of ST segment depression in the precordial leads during the acute inferior myocardial infarction was associated with greater myocardial necrosis and more frequent left coronary artery disease.

Vasospasm-induced polymorphic ventricular tachycardia

A 63-year-old man was admitted for workup of syncope and episodic, midsternal chest pain of one-year duration. During another episode of chest pain after admission, the electrocardiogram (Figure 1) revealed a heart rate of 55 beats/min; ST elevation in leads II, III and aVF; with reciprocal ST depression in leads I and aVL and upsloping ST depression in leads V1 to V4, demonstrating inferior and posterior wall myocardial ischemia. The telemetry rhythm strip (Figure 2) revealed ST elevation followed by wide-complex polymorphic ventricular tachycardia at 300 beats/min, characteristic of torsades de pointes that resolved 5 min later. Cardiac enzymes were within normal limits. Transthoracic echocardiography showed no ventricular dysfunction or wall motion abnormalities and cardiac catheterization revealed no evidence of stenotic coronary artery disease. These findings demonstrate polymorphic ventricular tachycardia in the setting of variant or Prinzmetal’s angina in the absence of obstructive coronary artery disease (1). The patient was subsequently treated with felodipine and a nitroglycerin patch to prevent episodes of variant angina, and reported no further episodes in six months of follow-up (2). Figure 1) Electrocardiogram revealing a heart rate of 55 beats/min; ST elevation in leads II, III and aVF, with reciprocal ST depression in leads I and aVL and upsloping ST depression in leads V1 to V4, demonstrating inferior and posterior wall myocardial ischemia ... Figure 2) Telemetry rhythm strips revealing ST elevation followed by wide-complex polymorphic ventricular tachycardia at 300 beats/min, characteristic of torsades de pointes that resolved 5 min later. Strip 1 Vasospasm; Strip 2 Polymorphism; Strip 3 Normal sinus ...