Postcoronary pain and the postmyocardial infarction syndrome

Since non-specific chest pain, which is a common feature after myocardial infarction, may be due to a mild form of Dressler's (postmyocardial infarction) syndrome 80 patients were studied after confirmed myocardial infarction. Two patients had clinical features of classical Dressler's syndrome with high erythrocyte sedimentation rates and strongly positive results for antimyocardial antibodies. Twenty three patients had non-specific chest pain; none had clinical features of Dressler's syndrome. There was no difference in the erythrocyte sedimentation rate between this group and the remainder who had no pain. Equal numbers in each group had weakly positive test results for antimyocardial antibodies; none had a strongly positive result. Thus there appears to be no evidence for a mild form of Dressler's syndrome, and the erythrocyte sedimentation rate and weakly positive results for antimyocardial antibodies are of no diagnostic value in Dressler's syndrome.     

Left ventricular pseudoaneurysm in a patient with Dressler's syndrome after myocardial infarction

Successful recanalisation of the left anterior descending coronary artery was performed in a 51 year old man who was admitted two weeks after acute anterior myocardial infarction. Fourteen days later, the patient developed Dressler's syndrome with cardiac tamponade, which was immediately punctured. Sternotomy was performed after two weeks because of progressive haemodynamic deterioration, and fibrinous masses were removed from the pericardium. The patient recovered but two weeks later echocardiography showed a perforation of the left ventricular free wall and formation of a pseudoaneurysm. Intensive monitoring showed significant enlargement of the pseudoaneurysm, which was subsequently resected. This case demonstrates that dangerous formation of a pseudoaneurysm can occur not only during the first days of acute myocardial infarction but also after weeks in patients suffering from non-infectious pericarditis caused by Dressler's syndrome. Although the incidence of Dressler's syndrome is declining, patients should be monitored carefully for several weeks, especially by echocardiography.

Keywords: Dressler's syndrome;  pseudoaneurysm;  myocardial infarction     

Postmyocardial infarction syndrome. Unusual mode of presentation

The postmyocardial infarction syndrome usually presents weeks after acute myocardial infarction as pericarditis associated with fever, leukocytosis, high sedimentation rate and pulmonary infiltrations. The unusual feature of the case discussed here was severe left shoulder pain resembling subdeltoid bursitis. Subsequently signs of pleuritis appeared prior to the classical picture of Dressler's syndrome. There was a dramatic response of steroid therapy.     

Constrictive pericarditis and anemia post myocardial infarction

A 67-year-old male presented with acute inferolateral myocardial infarction complicated by transient acute post infarction pericarditis. Six weeks later, he developed Dressler's syndrome associated with moderately severe anemia of chronic disease. Both of these resolved over the next few weeks, however, shortly thereafter, right sided congestive heart failure occurred. This progressed despite medical therapy and the diagnosis of constrictive pericarditis was made 10 months post infarction. Total pericardectomy was done one year after the onset of acute myocardial infarction with complete resolution of signs and symptoms.     

Myocardial infarction and late pericarditis]

The post-infarction syndrome was observed in 8 out of 138 consecutive patients with acute myocardial infarction; 24 other cases of the post-infarction syndrome diagnosed over the preceeding 3 years were also reviewed. In order to determine the clinical significance and the prognosis, this group of 32 was compared to another of 105 patients with myocardial infarction without pericarditis, with respect to age, sex, medical history and characteristics of the underlying necrosis (location and size). Several clinical signs are discussed. This study showed the post-infarction syndrome was associated with large infarcts, the course of which was marked by arrhythmias, conduction defects and haemodynamic problems. A considerable inflammatory syndrome was often observed. The relation between the post-infarction syndrome and early pericarditis is not proved; on the other hand, a close correlation between late pericarditis, atrial fibrillation and left pleural effusion was demonstrated. The long term prognosis of infarcts complicated by the post-infarction syndrome is without doubt determined by the size of the necrosis and by the presence of ventricular aneurysms which are frequently associated.     

Relation between the clinical course of acute myocardial infarction and specific sensitization of lymphocytes and lymphotoxin production

Seventy-eight patients with acute myocardial infarction (MI) were examined in order to assess the place of immune response caused by myocardial necrosis in the clinical pattern of the disease. The extent of autosensitization was estimated on the basis of E-RFC inhibition and lymphotoxin production in lymphocyte cultures in the presence of myocardial antigen. Sensitized lymphocytes emerge in the blood during the second week in primary acute MI, and during the first day in repeated acute MI. Patients with marked autosensitization more frequently developed recurrent anginal attacks and cardiovascular insufficiency; they were the only ones to show Dressler's syndrome and fatal outcomes. A positive correlation between cell sensitization and elevated IgG was seen during the third week of the disease. Lymphotoxin production tended to be increased in patients with repeated acute MI and Dressler's syndrome.     

Current incidence of postmyocardial infarction (Dressler''s) syndrome

This study examines the current incidence of postmyocardial infarction (Dressler's) syndrome. During 1980, 282 patients with documented myocardial infarction were admitted to our coronary care unit. Early postmyocardial infarction pericarditis was present in 18 patients (6.4%). Six of these patients received steroids and the remainder were treated with salicylates or other anti-inflammatory drugs. Anticoagulation was used in 149 patients (53%) during hospitalization. One hundred forty-four (51%) were receiving heparin and 133 (47%) received no anticoagulation. Information on the patient's status at 6 months was available in 229 patients who were discharged alive. Sixteen patients had died within 6 months after discharge and 4 patients were lost to follow-up study. There were no documented cases of Dressler's syndrome.

It is concluded that Dressler's syndrome has decreased in incidence and perhaps disappeared. This decrease is most likely related to decreased use of oral anticoagulants and to more aggressive treatment of postmyocardial infarction pericarditis.     

The clinical presentation of acute myocardial infarction predicts the severity of the lesion in the infarct-related artery

The purpose of this study was to correlate the clinical presentation of acute myocardial infarction with the patency rate and degree of residual stenosis of the infarct-related artery. One hundred and forty-five patients who underwent angiography after acute myocardial infarction were divided into two groups according to the time of onset of anginal pain prior to infarction. Group A comprised 119 patients, (109 men, 10 women, aged 53 +/- 9 years) who did not experience any symptoms before infarction or with anginal pain of less than 5 days preceding myocardial infarction, and group B 26 patients (all men, aged 54 +/- 12 years) with previous stable angina for greater than or equal to 1 year. Twenty-two days after acute myocardial infarction, 68 of the 145 patients (47%) had a patent infarct-related artery: 64 patients in group A (54%) and four patients in group B (15.4%) (P less than 0.006). Furthermore, 19 patients in group A (16%) and none in group B had less than 70% stenosis in the infarct-related artery (P less than 0.02). The mean residual stenosis in group A was 83.3 +/- 27% whereas in group B it was 98.1 +/- 4% (P less than 0.001). These results indicate that a long-standing history of angina before acute myocardial infarction is often related to a severe pre-existing atheromatous obstruction, which would account for the higher incidence of total coronary occlusion observed in group B. Thus angina of recent onset preceding acute myocardial infarction is associated with a higher patency rate of the infarct-related artery and frequent less than 70% residual lesions.     

Predictors of myocardial damage prior to hospital admission among patients with acute chest pain or other symptoms raising a suspicion of acute coronary syndrome

AIM: To evaluate factors which, prior to hospital admission, predict the development of acute coronary syndrome or acute myocardial infarction among patients who call for an ambulance due to suspected acute coronary syndrome. DESIGN: Prospective observational study. METHODS: All the patients who called for an ambulance due to suspected acute coronary syndrome in South Hospital's catchment area in Stockholm and in the Municipality of G?teborg between January and November 2000, were included. On arrival of the ambulance crew, a blood sample was drawn for bedside analysis of serum myoglobin, creatine kinase (CK)MB and troponin-I. A 12-lead electrocardiogram (ECG) was simultaneously recorded. RESULTS: In all, 538 patients took part in the survey. Their mean age was 69 years and 58% were men. In all, 307 patients (57.3%) had acute coronary syndrome and 158 (29.5%) had acute myocardial infarction. Independent predictors of the development of acute coronary syndrome were a history of myocardial infarction (P=0.006), angina pectoris (P=0.005) or hypertension (P=0.017), ECG changes with ST elevation (P<0.0001), ST depression (P<0.0001) or T-wave inversion (P=0.012) and the elevation of CKMB (P=0.005). Predictors of acute myocardial infarction were being a man (P=0.011), ECG changes with ST elevation (P<0.0001) or ST depression (P<0.0001), the elevation of CKMB (P<0.0001) and a short interval between the onset of symptoms and blood sampling (P=0.010). CONCLUSION: Among patients transported by ambulance due to suspected acute coronary syndrome, predictors of myocardial damage can be defined prior to hospital admission on the basis of previous history, sex, ECG changes, the elevation of biochemical markers and the interval from the onset of symptoms until the ambulance reaches the patient.     

Left ventricular aneurysmal repair within 30 days after acute myocardial infarction: early and mid-term outcomes

For safe resection, left ventricular aneurysmal repair after acute myocardial infarction is usually delayed. However, delaying surgery may not be possible or prudent in some patients who are clinically unstable after acute myocardial infarction. We retrospectively reviewed the early and mid-term outcomes of left ventricular aneurysmal repair in patients who had experienced acute myocardial infarction <30 days before the repair. From September 2001 through May 2006, 127 consecutive post-infarction patients underwent concurrent anteroapical left ventricular aneurysmal repair and coronary artery bypass grafting. In Group I (38 clinically unstable patients), the surgery was performed <30 days after myocardial infarction. In Group II, 89 patients underwent the surgery > or = 30 days after infarction. The mean follow-up period was 26.16 +/- 16.41 months. One Group I patient (2.6%) died in the hospital due to graft-versus-host reaction. Three Group II patients (3.4%) died: 2 of low cardiac output and 1 of multiple-organ failure. Hospital mortality rates were not statistically significant between groups (P=0.582). All patients required similar perioperative inotropic support, intra-aortic balloon pump support, and re-exploration for bleeding or cardiac tamponade. The actuarial survival rates were 94.7% (Group I) and 94.4% (Group II). Postoperative New York Heart Association functional class improved similarly in both groups. We infer that left ventricular aneurysmal repair with coronary revascularization < 30 days after a recent myocardial infarction is a feasible procedure, with acceptable morbidity and mortality rates. Our mid-term results were comparable with those for patients who underwent this surgery > or = 30 days after acute myocardial infarction.     

Systemic inflammatory markers in acute coronary syndrome: association with cardiovascular risk factors and effect of early lipid lowering

BACKGROUND: Evidence for statin therapy in prevention of coronary artery disease is overwhelming. In spite of theoretical benefits, any additional advantage of its early introduction in the management of acute coronary syndrome is, however, uncertain. We therefore investigated differences between plasma levels of the systemic inflammatory markers intercellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin, C-reactive protein and interleukin-6 in patients presenting with unstable angina or acute myocardial infarction, and assessed whether the 30-day levels of these markers are influenced by early instigation of the HMG-CoA reductase inhibitor pravastatin. MATERIALS AND METHODS: 170 (134 male) patients presenting with acute coronary syndrome, but without previous statin therapy, participated. Blood was taken within 24 h of onset of ischaemic pain and again at 30 days. In all, 87 (71 male) participants were treated with pravastatin (20-40 mg daily) and 83 (63 male) with a matched placebo. RESULTS: At presentation, interleukin-6 was higher in males than in females (P=0.008) and lower in those with a pre-existing history of myocardial infarction (P=0.038). C-reactive protein and interleukin-6 were greater in myocardial infarction, but this difference was lost at 30 days. Thirty-day changes in all parameters were inversely related to level at presentation but not to treatment with pravastatin. Hypertension (P=0.011) and smoking (P=0.042) were associated with elevation of C-reactive protein with no difference between unstable angina or acute myocardial infarction. The effect of these individual factors was cumulative. CONCLUSIONS: Interleukin-6 was greater in acute myocardial infarction than in unstable angina; E-selectin was positively associated with a previous myocardial infarction and inversely related to age. We found no effect of early introduction of pravastatin on systemic inflammatory markers 30 days after acute coronary syndrome.     

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)     

Prognostic value of cardiac troponin I in patients with non-ST elevation acute coronary syndrome

AIM: To elucidate relationship between initial blood levels of troponin I and occurrence of such events as death, myocardial infarction, coronary artery bypass surgery, and angioplasty in patients with non-ST elevation acute coronary syndrome. MATERIAL: One hundred one patients aged 32-78 years admitted to coronary care unit within 24 hours after onset of pain including 69 (68.3%) with unstable angina and 32 (31.7%) with non-ST elevation myocardial infarction. METHOD: Troponin I was determined by immunoassay, values below 0.4 ng/ml were considered normal. RESULTS. During 30 days of hospitalization there were 16 (35.5%) and 5 events (8.9%) events (p=0.001) among 45 patients who had elevated level of troponin I (group 1) and 56 patients with normal troponin I (group 2), respectively. By 6 months events occurred in 19 (42.2%) and 6 (10.7%) patients in groups 1 and 2, respectively (p=0.0004). CONCLUSION: Thus elevated blood level of troponin I in patients with non-ST elevation acute coronary syndrome has important value for prognosis.     

Dressler's syndrome following pulmonary vein isolation for atrial fibrillation

Dressler's syndrome, characterized by features of fever, pericarditis and pericardial effusion typically occurs in the weeks to months following a myocardial infarction. The syndrome has also been described following several other myocardial and pericardial pathologies, including two reports of Dressler's syndrome following radio-frequency ablation. We describe a case of Dressler's syndrome following a pulmonary vein isolation procedure, which is being performed with increasing frequency as a treatment strategy for atrial fibrillation.     

Acute febrile neutrophilic dermatosis (Sweet's syndrome) associated with post-myocardial infarction syndrome (Dressler's syndrome)

A case of Sweet's syndrome (acute febrile neutrophilic dermatosis) occurred in a patient with post-myocardial infarction syndrome (Dressler's syndrome). Although Sweet's syndrome has been described in association with leukemias, other malignant disorders, and a variety of chronic inflammatory disorders, it has not been reported associated with Dressler's syndrome. Sweet's syndrome is reviewed with regard to its associations and to its pathogenesis.     

Timely execution of the first stress test in patients with acute myocardial infarct

110 patients with acute myocardial infarction who survived the acute phase were individually randomized into the groups A and B. The two groups were identical with regard to age, sex, risk factors before the infarction, localization of the infarction, complications on the intensive care unit, therapy when being taken over from the intensive care unit and stay on the intensive care unit. With the same frequency in lethality (5.5% each) and morbidity (25.0% to 28.8%) the patients undergoing rehabilitation of group B significantly earlier underwent the first functional test (20.5 +/- 8.4 to 32.7 +/- 10.8 days). In group B this was possible in 21% of the patients after 2 weeks, in 46% after 3 weeks and in 21% after 4 weeks. An age over 60 years, the heart insufficiency in the acute phase and a dilated or dyskinetic left ventricle at the end of the acute phase had a prolonging effect on the provisional plan of time, when the patient was taken over from the intensive care unit. Of the complications during the rehabilitation phase I particularly Dressler's syndrome and the heart insufficiency prolonged the time up to the first functional test, whereas haemodynamically ineffective disturbances of rhythm show an insignificant influence.     

Role of perceptive threshold in myocardial infarction patients without previous angina

The purpose of this study is to clarify the mechanism of sudden onset myocardial infarction (MI) without previous angina and the relationship of MI without previous angina to the mechanism of onset of postinfarction asymptomatic myocardial ischemia. The mean initial time of ischemic pain in the upper arm under the tourniquet test was significantly prolonged in the MI patients without previous angina, compared with that for the MI patients with previous angina and normal control subjects, although there are some overlapping cases (74 +/- 37 sec versus 52 +/- 20 sec (p less than 0.01), and versus 56 +/- 15 sec (p less than 0.05), respectively). The tolerance time for ischemic pain also was similarly prolonged. There was no significant difference between the groups of MI patients (with and without previous angina) with respect to age, frequency of complications of diabetes mellitus, severity of coronary artery lesions or site of MI. The incidence of post-infarction myocardial ischemia was 50% for the previous angina group and 39.5% for the group without previous angina, but the frequency of asymptomatic ischemia was significantly higher in patients without previous angina, at 66.7%, than in those with previous angina, 32.3% (p less than 0.05). These results suggest that there is a close relationship between the mechanism of MI with sudden onset and that of asymptomatic myocardial ischemia during the pre- and post-infarction periods in patients with low sensitivity to pain.     

Transient retinopathy after acute myocardial infarction treated by reperfusion therapy: clinical background and manifestation

OBJECTIVES: The severe inflammatory reaction caused by acute myocardial infarction and reperfusion affects both the heart and other remote organs. The occurrence of retinopathy was evaluated in patients with acute myocardial infarction who underwent reperfusion therapy. METHODS: We investigated 29 patients with first acute myocardial infarction who underwent successful reperfusion therapy within 24 hr of the onset. Ophthalmic examinations including visual acuity test and ocular fundoscopy were performed within 3 days, 2 weeks, and then monthly up to 3 months after the onset of acute myocardial infarction. Plasma levels of intercellular adhesion molecule-1(ICAM-1), interleukin-6 and high sensitivity C-reactive protein were measured on admission. RESULTS: Soft exudates around the optic disc appeared in 17(58.6%) of the 29 patients, among whom 5 also developed superficial hemorrhages(17.2%). The retinopathy became most remarkable between 1 to 2 months after the onset of acute myocardial infarction and then faded away without any specific treatment. None of the patients had impairment of visual acuity, although 4 of the 17 patients with retinopathy complained of either blurred vision or metamorphopsia. Hypertension and/or diabetes mellitus tended to be more common in the retinopathy group than in the non-retinopathy group(59% vs 33%, p = 0.096). Plasma ICAM-1 levels were significantly higher than in the non-retinopathy group than in the retinopathy group(p = 0.017). There was no significant difference in plasma levels of interleukin-6 and high sensitivity C-reactive protein between the two groups. CONCLUSIONS: Retinopathy may occur after reperfusion for acute myocardial infarction. The dominant manifestation is transient soft exudates reflecting spotty retinal ischemia, probably due to microvascular obstruction.     

Electrophysiologic actions and antifibrillatory efficacy of subacute left stellectomy in a conscious, post-infarction canine model of ischemic ventricular fibrillation

The autonomic nervous system appears to modulate ventricular arrhythmias associated with acute myocardial ischemia. This study investigated the electrophysiologic effects and antifibrillatory actions of subacute left stellectomy in a conscious, post-infarction canine model of sudden cardiac death. Twenty-two dogs with a previous anterior wall myocardial infarction and inducible ventricular arrhythmias were randomized to undergo either left stellectomy (n = 12) or remain as sham-denervated controls (n = 10). Five to 7 days post left stellectomy, there were no significant changes in heart rate, electrocardiographic intervals or ventricular refractoriness compared to sham-denervated controls. Acute posterolateral ischemia was produced in left stellectomy and sham-denervated dogs by anodal current-induced thrombosis via a previously positioned electrode in the left circumflex coronary artery. Ventricular fibrillation developed within 1 hour of the onset of ischemia (early ventricular fibrillation) in 3/12 (25%) left stellectomy dogs versus 8/10 (80%) sham-denervated controls (P less than 0.05). However, 24-hour mortality rate was 5/12 (42%) after left stellectomy versus 8/10 (80%) after sham denervation (P = 0.072). Small differences in regional myocardial norepinephrine content, which is a marker for neuronal integrity, occurred in the mid-posterolateral and mid-anteroseptal regions of the left ventricle after left stellectomy. Overall norepinephrine concentration after left stellectomy was 409.70 +/- 9.90 ng/g vs 428.07 +/- 10.84 ng/g in sham controls (P = NS). In summary, subacute left stellectomy significantly reduces the incidence of ventricular fibrillation occurring within 1 hour of the onset of acute posterolateral ischemia at a distance to a previous myocardial infarction in conscious dogs, and tends to reduce the ischemic post-infarction mortality at 24 hours after the onset of ischemia. This protective effect of left stellectomy is not due to any alteration in cardiac electrophysiologic parameters measured prior to the development of acute posterolateral ischemia, nor is it related to regional denervation as determined by myocardial tissue concentration of residual norepinephrine.     

Natural history of late potentials in the first ten days after acute myocardial infarction and relation to early ventricular arrhythmias

Serial signal-averaged electrocardiograms (ECGs) were performed every 48 hours in 50 patients admitted to the coronary care unit with acute myocardial infarction. The prevalence of late potentials was 32% at presentation (mean time to recording 12.4 +/- 6.6 hours after onset of chest pain) and increased progressively throughout the hospital stay. New late potentials were recorded in patients with no prior acute myocardial infarction as early as 3 hours after the onset of chest pain and as late as 8 days. Late potentials appeared transiently in only 3 patients. The detection of late potentials in the initial signal-averaged ECG identified patients with clinically significant early ventricular arrhythmias with a sensitivity of 80% and specificity of 72%. The predictive accuracy was 38% for a positive test and 94% for a negative test. Patients with early ventricular arrhythmias had significantly lower voltage in the terminal 40 ms of the filtered QRS complex (16 +/- 8 vs 32 +/- 19 microV, p less than 0.01) than those without arrhythmias. The signal-averaged ECG may be useful in identifying patients at high risk of developing clinically significant early ventricular arrhythmias after acute myocardial infarction.