Post-cardiac injury syndrome following transvenous pacing: Case report

Post-cardiac injury syndrome (PCIS) is an inflammatory process involving the pericardium secondary to cardiac injury. It can develop after cardiac trauma, cardiac surgery, myocardial infarction, and, rarely, after certain intravascular procedures. We report a rare case of an iatrogenic cardiac rupture followed by PCIS with delayed inflammatory pericardial effusion after pacemaker implantation. A comprehensive literature review on this topic is provided.     

The postcardiac injury syndromes.

Late pericarditis following myocardial infarction, cardiac surgery, or trauma is referred to as postmyocardial infarction syndrome (PMIS) or postcardiotomy syndrome (PCS), respectively. The term postcardiac injury syndrome (PCIS) is used to encompass both these entities. PCIS is characterized by fever, pleuropericardial pain, pericarditis, and pulmonary involvement. Abnormal laboratory findings include leukocytosis, high sedimentation rate, and chest x-ray abnormalities of pleural effusion with or without pulmonary infiltrates. Evidence supports an immunopathic etiology; viruses may play a contributing role. The course is benign but rare complications include tamponade, constriction, anemia, and coronary bypass graft occlusion. Anti-inflammatory agents are helpful; indo-methacin and steroids are preferably avoided. Rarely, PMIS-like syndrome may occur following pulmonary embolism. Anticoagulation and steroids have been used successfully in the latter situation.     

The postcardiac injury syndrome following percutaneous transluminal coronary angioplasty

A 57-year-old man, who had suffered an anterior Q-wave myocardial infarction complicated with typical postcardiac injury syndrome (PCIS) 9 years earlier, underwent percutaneous transluminal coronary angioplasty (PTCA) without any immediate clinical, laboratory, or radiological signs of complications. After 4 days he recognized the recurrence of the earlier symptoms of PCIS. The diagnosis was supported by slight fever, elevated inflammatory parameters, and improvement when oral corticosteroids were given. The observations suggest that milder cardiac injury than previously considered, that is, without demonstrated structural damage to pericardium or myocardium, may precipitate PCIS in predisposed individuals. The case adds a differential diagnosis to chest pain and malaise following PTCA.     

Post-cardiac injury syndrome and an increased humoral immune response against the major contractile proteins (actin and myosin)

To better understand the pathogenesis of the post-cardiac injury syndrome (PCIS) 2 models of cardiac injury were studied. One hundred twenty-nine patients who underwent cardiac surgery and 80 patients with acute myocardial infarction (AMI) were prospectively followed and the levels of anti-heart antibodies (AHA), anti-actin antibodies (AAA) and anti-myosin antibodies (AMA) were determined. In the surgical group, PCIS developed in 27 patients (21%) and incomplete PCIS in 36 (28%). In the AMI group, PCIS did not develop in any patient, but incomplete PCIS developed in 11 patients (14%) (p less than 0.001). The surgical group showed a significantly higher humoral immune response than the AMI group when analyzed for AHA and anti-contractile protein antibodies. After cardiac surgery, AHA developed in 59 patients (46%), AAA developed in 33 (26%) and AMA developed in 49 (38%); in the AMI group, significant levels of AHA, AAA and AMA developed in 16 (20%), 7 (9%) and 13 patients (16%), respectively. These studies show a significant correlation between the PCIS clinical classification and auto-antibodies raised against heart contractile proteins.     

Pseudo Wellens T-waves in patients with suspected myocardial infarction: how cardiac magnetic resonance imaging can help the diagnosis

Wellens' syndrome is characterized by symmetrically inverted T-waves in the precordial leads suggestive of impending myocardial infarction due to a critical proximal left anterior descending (LAD) stenosis. We describe three unusual cases of patients with such electrocardiographic abnormality in which coronary angiography ruled out the presence of critical coronary stenosis and cardiac magnetic resonance imaging excluded the presence of acute or chronic myocardial infarction.     

Paroxysmal atrioventricular block and right coronary artery stenosis without acute myocardial infarction

Tako-Tsubo Cardiomyopathy (TTC) is described as transient left ventricular (LV) dysfunction without coronary artery stenoses. Typically the onset of TTC-syndrome is following emotional or physical stress. As an acute cardiac syndrome it is mimicking ST-elevation myocardial infarction. In this case we report from a 73-year old woman presenting with cardiac arrest after a long-distance bus-tour, and ongoing resuscitation to our ICU. Advanced life support with temporary ventricular pacing was continued until onset of stable spontaneous circulation. Left ventricular angiography revealed normal coronary arteries and the typical apical ballooning phenomenon. Echocardiographic findings resolved completely within 10 days. The patient survived, achieved good cerebral recovery (CPC 1) and was alert and fully oriented on discharge after 18 days.     

Pleural effusions following cardiac injury and coronary artery bypass graft surgery

This article discusses the pleural effusions that occur with the post-cardiac injury (Dressler's) syndrome (PCIS) and those that occur after coronary artery bypass graft (CABG) surgery. The PCIS can occur after any type of cardiac injury and is thought to be due to anti-myocardial antibodies. The primary symptoms are fever and chest pain, and pericarditis is frequently present. Pleural effusions are common with PCIS. The primary treatment for PCIS is a nonsteroidal anti-inflammatory agent or corticosteroids. Following CABG surgery, most patients will have a small unilateral left-sided pleural effusion, and approximately 10% of patients will have a larger effusion. These large effusions can be separated into early effusions occurring within the first 30 days of surgery that are bloody exudates with a high percentage of eosinophils, and late effusions occurring more than 30 days after surgery that are clear yellow lymphocytic exudates. The primary symptom of a patient with a pleural effusion post-CABG surgery is dyspnea; chest pain and fever are uncommon. Most patients with large pleural effusions postCABG surgery are managed successfully with one to three therapeutic thoracenteses.     

Late left ventricular pseudoaneurysm formation following subacute myocardial infarction

We describe a patient with a subacute inferior myocardial infarction who developed a pseudo-aneurysm more than 18 days after the acute event. This is an unusual case with three different complications of a myocardial infarction: Firstly, ventricular rupture is usually the result following transmural myocardial infarction without reperfusion. However, coronary angiography confirmed reperfusion after late thrombolysis in this patient. The subacute rupture could potentially be caused or aggravated by the late thrombolysis. Secondly, this patient developed a mural apical thrombus in a non-infarcted region. It seems most likely that the new infarct caused a low flow state which enhanced thrombus formation. Against expectations, this developed at the apex rather than the site of the recent inferior wall myocardial infarction. Thirdly, we documented the development of a pseudo-aneurysm more than 18 days after the myocardial infarction. This complication is rarely seen at this stage after a myocardial infarction, as most pseudo-aneurysms are formed within 7 days after a myocardial infarction. We have beautifully visualised the apical thrombus and pseudo-aneurysm with echocardiography. This report shows that serial echocardiography is a very useful tool in evaluating the patient's clinical and cardiac status in the period after a myocardial infarction.     

Natural history of combined right bundle branch block and left anterior hemiblock (bilateral bundle branch block)

One hundred fifteen patients with combined right bundle branch block (RBBB) and left anterior hemiblock (LAH) were separated into two groups depending upon whether RBBB and LAH was associated with acute myocardial infarction (group I, 32 patients) or was a chance electrocardiographic finding (group II, 83 patients).In 10 patients in group I complete heart block developed and in six patients high grade second degree atrioventricular (A-V) block developed. The incidence of serious arrhythmia was twice and mortality was three times the average for the coronary care unit (CCU).The majority of patients in group II had clinical evidence of advanced myocardial disease as manifested by congestive heart failure, healed myocardial infarction and left ventricular dyskinesia. During a cumulative observation period of 262 patient years, complete heart block developed in only two patients, whereas second-degree A-V block of sufficiently high degree to necessitate permanent cardiac pacing developed in three patients.It is concluded that (1) combined RBBB and LAH usually reflects advanced myocardial disease, (2) the clinical course is determined more by the myocardial disease than by the conduction disorder, (3) prophylactic cardiac pacing is not warranted in chronic RBBB and LAH, and (4) cardiac pacing has little impact on mortality when RBBB and LAH are associated with acute myocardial infarction.     

Acute myocardial infarction as the presenting symptom of acute myeloblastic leukemia with extreme hyperleukocytosis

This case report deals with an unusual leukostatic complication in a 56-year-old woman with acute myeloblastic leukemia (AML) and extreme hyperleukocytosis (316 x 10(9)/L) who presented with acute myocardial infarction (MI). After leukopheresis the patient achieved hemodynamic stabilization and rapid neurologic recovery of encephalopathy that had also developed after the infarction. Considering the central role of WBC in the remodeling of post MI myocardial tissue, it was obvious that administration of chemotherapy with its subsequent inevitable pancytopenia could impose an increased risk for further cardiac complications including myocardial rupture. Nevertheless, cytarabine-based induction chemotherapy was initiated 3 days after admission, and she achieved prolonged complete remission. Coronary angiography disclosed segmental atherosclerosis, but the only significant obstruction was in the right coronary artery. The patient died with relapsed leukemia 7 years later without recurrence of any cardiac symptoms or signs. Autopsy disclosed segmental coronary atherosclerosis involving the LAD (60% obstruction), suggesting that atherosclerosis was a predisposing risk factor. Additional compromise to blood perfusion due to leukostasis had led to this unusual complication of AML involving a major vessel. This is the first documented case of leukostasis causing coronary artery occlusion as well as the first report of successful induction chemotherapy for AML during a myocardial infarction.     

Clinical outcomes following "rescue" administration of abciximab in patients undergoing percutaneous coronary angioplasty

Pre-intervention administration of abciximab in patients at "high risk" for coronary angioplasty has been shown to reduce acute and long-term cardiac outcomes. The role of intra-procedural ("rescue") administration of abciximab has not been fully elucidated. We assessed the clinical outcomes associated with rescue administration of abciximab during complex percutaneous coronary interventions. We studied in-hospital and long-term (1-year) outcomes (death, myocardial infarction and target lesion revascularization) of 298 consecutive patients (78% male; age, 62 +/- 11 years; 83% with acute coronary syndrome) treated with abciximab for thrombus-containing lesions, sub-optimal angioplasty results, procedural dissections or other complications. Stents were used in 73% of procedures. Procedural success was 97.0% and overall major in-hospital complication rate was 3.0% (death, 1.3%; Q-wave myocardial infarction, 0.7%; and emergent bypass surgery, 1.0%). Most frequent angiographic complications included visible thrombus (17%), dissections (17%), threatened closure (7%), and distal embolization (7%). In-hospital non-Q wave myocardial infarction (defined as CK-MB 5 times normal) occurred in 31.0%. Out-of-hospital to one-year events included death (1.7%), Q-wave myocardial infarction (2.7%), and target lesion revascularization (15.1%); cardiac event-free survival was 82.9%. We conclude that rescue administration of abciximab is associated with relatively low in-hospital complications and favorable long-term outcome in patients with sub-optimal angioplasty results and/or procedure-related complications, although peri-procedural non-Q wave myocardial infarction rate is high. A clinical and cost-effective comparison between provisional and rescue administration of abciximab may be warranted.     

Pheochromocytoma presenting with Takotsubo syndrome

The clinical presentation of Takotsubo syndrome, or apical ballooning syndrome, resembles an extensive anterolateral myocardial infarction with chest pain symptoms and electrocardiographic ST-elevation or T-wave inversion noted in most patients. However, coronary arteries are invariably found to be normal or to display minimal atherosclerotic disease despite modest elevation of cardiac enzymes. Since most cases of Takotsubo syndrome occur after intense physical and/or emotional stress, catecholamine surge appears to be a common underlying mechanism. We present a case of Takotsubo syndrome, which presented with unusual symptoms and was found to be caused by pheochromocytoma. A sudden rise in blood pressure moments after completion of echocardiographic stress testing aided in uncovering the diagnosis.     

Evolving considerations in the management of patients with left bundle branch block and suspected myocardial infarction

Patients with a suspected acute coronary syndrome and left bundle branch block (LBBB) present a unique diagnostic and therapeutic challenge to the clinician. Although current guidelines recommend that patients with new or presumed new LBBB undergo early reperfusion therapy, data suggest that only a minority of patients with LBBB are ultimately diagnosed with acute myocardial infarction, regardless of LBBB chronicity, and that a significant proportion of patients will not have an occluded culprit artery at cardiac catheterization. The current treatment approach exposes a significant proportion of patients to the risks of fibrinolytic therapy without the likelihood of significant benefit and leads to increased rates of false-positive cardiac catheterization laboratory activation, unnecessary risks, and costs. Therefore, alternative strategies to those for patients with ST-segment elevation myocardial infarction are needed to guide selection of appropriate patients with a suspected acute coronary syndrome and LBBB for urgent reperfusion therapy. In this article, we describe the evolving epidemiology of LBBB in acute coronary syndromes and discuss controversies related to current clinical practice. We propose a more judicious diagnostic approach among clinically stable patients with LBBB who do not have electrocardiographic findings highly specific for ST-segment elevation myocardial infarction.     

Multiple cardiac papillary fibroelastoma and transient left ventricular apical ballooning syndrome in an elderly woman: case report

An elderly Japanese woman presented with evidence of a myocardial infarction. Emergency angiography showed no significant atherosclerotic disease, but the anterior and anteroseptal walls were akinetic, with 'ballooning' of the apex. She was suspected to have transient left ventricular apical ballooning syndrome (TLVABS). Two months later, transthoracic echocardiography showed normal left ventricular wall motion and function, together with a 5-mm cardiac papillary fibroelastoma (CPF) attached to the aortic valve. Transesophageal echocardiography showed a stalked CPF on the aortic side of the left coronary cusp, and a smaller CPF on the right coronary cusp. It was hypothesized that the CPF caused the TLVABS through myocardial stunning. This may occur as a result of transient dynamic ostial occlusion by the fibroelastoma, or because of emboli from the fibroelastoma which then subsequently spontaneously lysed. This syndrome may represent an unusual manifestation of transient cardiac ischemia. Whilst TLVABS has been mainly reported in Japanese patients, more recent studies have suggested that other populations might also be affected.     

Coronary blood flow in patients with cardiac syndrome X

BACKGROUND: Epicardial coronary arteries are normal in patients with cardiac syndrome X. It is, however, unclear whether there is an abnormality at the level of microvascular circulation. In this study, our aim was to evaluate the epicardial coronary blood flow and myocardial perfusion in patients with cardiac syndrome X. METHODS: Two hundred and three patients (mean age 53+/-10 years, 85 men) were included in the study. The diagnosis of cardiac syndrome X was made in patients who had a complaint of typical anginal chest pain and had ischemic findings on either myocardial perfusion scintigraphy or a treadmill exercise test, and whose coronary angiograms did not reveal any pathology. Fifty patients (mean age 54+/-11 years, 24 men) who had a complaint of typical anginal chest pain and had a normal myocardial perfusion test and normal coronary arteries were recruited as the control group. Epicardial coronary blood flow was evaluated with the thrombolysis in myocardial infarction frame count method and myocardial perfusion was evaluated with the myocardial blush grade method. A myocardial blush grade of < or =2 in any vessel was considered abnormal. RESULTS: Although the right coronary thrombolysis in myocardial infarction frame count was higher in patients with syndrome X (14.9+/-7.6 vs. 11.7+/-4.4 in controls; P=0.014), there were no statistically significant differences between the groups in terms of mean thrombolysis in myocardial infarction frame count in the coronary arteries. Abnormal myocardial blush grade was present in 85 patients (42.3%) with syndrome X, and in 17 patients (34.7%) in the control group (P>0.05). CONCLUSION: We found that the epicardial coronary blood flow, as assessed by thrombolysis in myocardial infarction frame count, and myocardial perfusion, as assessed by myocardial blush grade, were normal in patients with cardiac syndrome X.     

Pericardial involvement in acute myocardial infarction

The incidence of both early postinfarction pericarditis and post-myocardial infarction (Dressler's syndrome) appears to be declining. Pericardial pain and pericardial friction rub define early postinfarction pericarditis and usually develop on day 2 or 3 after a transmural myocardial infarction. The clinical course is benign, and the prognosis of the patient is not altered by development of this complication. Pericardial effusions have been found in as many as 28% of patients after acute MI. Asymptomatic pericardial effusions do not require specific therapy nor do they absolutely contraindicate the use of anticoagulation as was previously thought. The preferred form of therapy for early postinfarction pericarditis is aspirin. Avoidance of corticosteroids and NSAIDs must be considered carefully because of the reported complications of these agents. The post-myocardial infarction syndrome develops usually during the second or third week after acute MI but may be seen as early as 24 hours and as late as several months after the MI. Whether this syndrome is the result of autosensitization to myocardial antigens released into the circulation during infarction remains uncertain. Alternative hypotheses for the causation of the syndrome include the release of blood in the pericardial space and simply that the syndrome represents a prolonged and exaggerated form of early postinfarction pericarditis. Clinically, post-myocardial infarction syndrome is manifested by fever, malaise, chest pain, and the presence of a pericardial and possibly pleuropericardial friction rub. Pericardial effusion is frequently large, and, rarely, cardiac tamponade may develop and require pericardiocentesis. Treatment consists of aspirin, NSAIDs, or corticosteroids.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prinzmetal angina. Multifocal ischemia, recurrent AV block, and bradycardia with patent coronary arteries responsive to verapamil

Coronary vasospasm may result in recurrent angina pectoris and cause acute myocardial infarction. The extent to which the "sudden death syndrome" occurs is unknown. The case described herein is unique in that the clinical features, including hypotension, AV block, and ventricular arrhythmias, were similar to those seen in myocardial infarction with a poor prognosis, yet infarction was not documented. In subsequent, long-term follow-up evaluation, chest pain has been recurrent, but despite close observation, no further major cardiac complications have been documented. Long-term use of verapamil has contributed to better control of clinical symptomatology.     

Uncommon cause of complicated myocardial infarction with normal coronary arteries in a Saudi patient

A case of a young Saudi patient with a previous diagnosis of bronchial asthma, nasal polyps, and chronic smoker, presented with atypical chest pain, elevated serum troponin and borderline ischemic electrocardiogram (ECG) changes, with no significant regional wall motion abnormalities at bedside echocardiography is reported. The patient was admitted to the coronary care unit for continuous monitoring as possible acute coronary syndrome, non-ST elevation myocardial infarction (STEMI). One hour after admission, the patient had ventricular fibrillation (VF) cardiac arrest that required three DC shocks and amiodarone bolus before returning of spontaneous circulation, which followed the fourth shock. The resuscitation took 15 minutes of cardiopulmonary resuscitation (CPR). An immediate 12-leads ECG showed significant ST elevation in precordial leads that mandate an urgent coronary angiogram that revealed patent coronary arteries, therefore spasm of normal coronary arteries was postulated as the operative factor. The cardiac magnetic resonance image (MRI) showed a picture of transmural anterior myocardial infarction, which correlates with the follow up echocardiogram reporting hypokinetic anterior wall. A complete history was taken and no use of illicit drugs or alcohol was found. The unusual presentation in such a patient with evidence of extensive anterior STEMI and normal coronary arteries raise the thought of considering uncommon causes. In view of previous medical history and laboratory evidence of eosinophilia, Kounis syndrome was considered dominant in the differential diagnosis.     

Postpericardiotomy and postmyocardial infarction syndrome presenting as noncardiac pulmonary edema

Three cases are reported that describe acute pulmonary edema as an early manifestation of a postpericardiotomy or postmyocardial infarction syndrome. Each of these cases occurred in the presence of good left ventricular function. The cases suggest this syndrome occurs in immunologically primed patients who have had prior cardiac injury resulting in readily available heart antibody. The first report followed an acute myocardial infarction that required a temporary pacemaker, and the two other cases occurred following coronary artery bypass surgery. Two of the patients had a history of distant myocardial or pericardial injury, and the third patient had an acute anteroseptal myocardial infarction two to three weeks before cardiac surgery. All three patients with pulmonary edema responded dramatically to corticosteroids, having been resistant to diuretic and pre-load and afterload reduction therapy, suggesting an autoimmune capillary injury process. Early recognition of such a syndrome is important since all three patients were successfully treated, and might otherwise have been confused with other causes of pulmonary edema.     

Dilated cardiomyopathy and myocardial infarction secondary to congenital generalized lipodystrophy

Congenital generalized lipodystrophy, also known as Berardinelli-Seip syndrome, is a very rare hereditary syndrome that is characterized by an almost complete absence of adipose tissue from birth. Cardiac involvement seems to have substantial influence in the long-term prognosis. Herein, we report an apparently unique case of congenital generalized lipodystrophy with cardiac sequelae. A 17-year-old woman, diagnosed in childhood with Berardinelli-Seip syndrome, presented with severe epigastric pain that was secondary to previous myocardial infarction. The patient had ischemia, dilated cardiomyopathy, and congestive heart failure, but no coronary artery disease. She was discharged from the hospital in stable condition after 3 days of medical treatment. To our knowledge, this is the 1st reported case of congenital generalized lipodystrophy with dilated cardiomyopathy, congestive heart failure, severe mitral regurgitation, and inferior myocardial infarction as cardiac sequelae of this syndrome--but without evidence of coronary artery disease or cardiac hypertrophy. In addition to discussing this patient's case, we present diagnostic and therapeutic approaches to Berardinelli-Seip syndrome.