Percutaneous transluminal coronary angioplasty in acute myocardial infarction

Percutaneous transluminal coronary angioplasty (PTCA) has, in general, been restricted to therapy for patients with angina pectoris. Thrombolytic therapy and guide wire recanalization have been used to recanalize coronary arteries in patients with evolving myocardial infarction. Recently we and others have examined the use of PTCA to recanalize the acutely occluded artery associated with the early evolving phase of myocardial infarction. PTCA was performed as definitive therapy in eight patients with acute myocardial infarction. Seven of these had totally occluded arteries to the region of infarct. The infarct-related artery was open within 20 minutes in each of these cases. PTCA recanalization resulted in evidence for reperfusion in each case. Residual stenoses either were not present or were minimal. The procedure was well tolerated. These preliminary results suggest that PTCA may be a reasonable alternative to intracoronary thrombolytic therapy in certain patients with acute evolving myocardial infarction.     

Percutaneous transluminal coronary angioplasty in evolving acute myocardial infarction

In 29 patients with evolving acute myocardial infarction, acute reperfusion of the infarct-related coronary artery was attempted using percutaneous transluminal coronary angioplasty (PTCA). Before PTCA, angiography showed 23 totally occluded and 6 severely stenotic infarct-related coronary arteries. PTCA was initially successful in 25 of 29 patients (86%). Reocclusion occurred in 4 patients within 12 hours after successful PTCA and was associated with new electrocardiographic changes or recurrence of symptoms. In 17 patients the infarct-related coronary artery remained patent at early follow-up; late stenosis occurred in 4 patients. Recurrence of stenosis was accompanied by development of angina. No clinical or angiographic features distinguished those with ultimate vessel patency, occlusion or recurrence of stenosis. On follow-up, ventricular function appeared better preserved or improved in those with a patent infarct-related coronary artery than in those with an occluded infarct-related coronary artery. Further studies are warranted to compare PTCA and streptokinase as primary reperfusion modalities in evolving acute myocardial infarction.     

Myocardial infarction in young people with normal coronary arteries

Myocardial infarction occurring in young people with angiographically normal coronary arteries is well described but the pathophysiology of this condition remains unknown. Coronary artery spasm in association with thrombus formation and minimal atheromatous disease or spontaneous coronary artery dissection are possible causes. Two young men presented with severe chest pain after acute alcohol intoxication and each sustained an extensive anterior myocardial infarction. Investigations including intravascular ultrasound showed no evidence of atherosclerotic coronary artery disease. Coronary artery spasm associated with acute alcohol intoxication as well as a prothrombotic state and endothelial damage related to cigarette smoking may be mechanisms leading to acute myocardial infarction in these cases. Acute myocardial infarction occurs in young persons with normal coronary arteries and the diagnosis should be considered in young patients presenting with severe chest pain, particularly those abusing cocaine or alcohol, so that reperfusion therapy can be initiated promptly.

Keywords: myocardial infarction;  coronary vasospasm;  alcohol;  intravascular ultrasound     

The role of coronary thrombosis in myocardial infarction: further evidence shown by intracoronary thrombolysis with streptokinase

Myocardial infarction is usually caused by a thrombus occurring on a significant coronary lesion. A 60-year-old male was admitted with an acute evolving anterior myocardial infarction. Three hours after the beginning of chest pain, the electrocardiogram showed ST-segment elevation in the anterior and lateral leads which persisted despite intravenous nitroglycerin (100 mcg/min). One hour later, an angiogram showed complete obstruction at the origin of the left anterior descending artery (LAD). After intracoronary streptokinase (250,000 units) the LAD opened and a 90% obstruction was seen at its origin. However, an anterior myocardial infarction occurred. One month later, an angiogram showed a slight irregularity at the origin of the LAD. Thus, this case demonstrates that 1) a myocardial infarction may occur with a near normal coronary artery, and 2) a thrombus may occur at the site of a slight coronary irregularity.     

Surgical treatment of acute myocardial infarction

In 1989 the following indications for surgical treatment of acute myocardial infarction are: (1) acute evolving myocardial infarction less than 6 h from onset, in patients in whom percutaneous transluminal coronary angioplasty (PTCA) or streptokinase (SK), depending on the coronary anatomy, has been unsuccessful; if single vessel disease, coronary artery bypass grafting (CABG) is unlikely; if multiple vessel disease, CABG is preferable to SK/PTCA unless a very major 'culprit' lesion can be identified with certainty; (2) postinfarction angina hours to days after a transmural myocardial infarction unyielding to maximal medical therapy and in patients with a coronary artery obstruction not amenable to PTCA; (3) occlusion of a coronary artery during cardiac catheterization that cannot be fixed by PTCA and/or SK; (4) occlusion of a coronary artery during PTCA causing hemodynamic obstruction and a threatened myocardium subtended by the obstructed coronary artery; (5) balloon-dependent patients in cardiogenic shock without mechanical defects who have adequate residual left ventricular function as determined by regional wall motion studies; (6) ventricular septal defect secondary to myocardial infarction unless there is terminal organ damage; (7) mitral valve replacement with coronary bypass for acute papillary muscle rupture; (8) semi-emergency cardiac transplantation, either with or without a mechanical bridge to transplant in young individuals (less than 50 years) who have suffered massive destruction of left ventricular myocardium by an acute coronary occlusion with or without recurring ventricular tachyarrhythmias. Ejection fraction in this clinical category is always under 0.20 and usually under 0.15.     

Thrombolytic therapy in acute myocardial infarct

Numerous studies have demonstrated a high prevalence of coronary thrombi in the early hours of acute myocardial infarction leading to a complete occlusion of the coronary artery. Thrombolysis and reperfusion in the very early hours can preserve jeopardized myocardium from necrosis. Using intravenous streptokinase early reperfusion can be achieved in 50% of the patients with occluded coronary arteries. Using rt-PA and prourokinase reperfusion rate is 60 to 70%. Both agents have more fibrin-specific activity, therefore the risk of bleedings is reduced. However, thrombolytic treatment with early reperfusion seems to be just the first step. Further procedures (percutaneous transluminal coronary angioplasty = PTCA or early bypass surgery) have to be added to improve not only the short-term but also the long-term prognosis. If the ongoing randomized trials confirm a significant reduction in mortality due to reperfusion and improved ventricular function this "aggressive treatment" of the evolving myocardial infarction will change our strategy from a symptomatical to a more causal therapy.     

Emergency surgical revascularization in establishing myocardial infarctions. Treatment of subtotal coronary occlusions

The introduction of intracoronary thrombolysis as a treatment for myocardial infarction has led to an increase in the number of very early coronary angiographies carried out in the acute phase of myocardial infarction. These investigations can be performed without excessive risk. In some cases, severe stenosis with significant distal circulatory impairment without evidence of thrombosis is found. In these very early investigations, these findings may represent a "pre-thrombolic" lesion in an evolving myocardial infarction. Six cases of very severe pre-thrombolitic stenosis of the LAD were observed in a series of 67 coronary angiographies performed in the early stages of myocardial infarction. These six cases were selected on strict clinical, ECG and angiographic criteria. One patient was hospitalised with cardiogenic shock. The six patients underwent emergency coronary bypass surgery: average time from admission to coronary angiography was 55 minutes; average time from coronary angiography to surgery was 3 hours. These 6 pre-thrombolic lesions of the LAD were also associated with lesions of the left circumflex and right coronary arteries. There were no operative complications but two patients had stormy immediate postoperative periods. There was no hospital mortality. All patients were reinvestigated at 1 month and all grafts were shown to be patent. The left ventricular ejection fractions improved in 3 cases, remained unchanged in 2 cases, and deteriorated in 1 case (the patient with cardiogenic shock). These results suggest that emergency coronary bypass surgery is a rational treatment of pre-thrombolic coronary stenosis observed at early coronary angiography in patients with evolving myocardial infarction in order to preserve as much myocardial muscle as possible.     

Out-of-hospital coronary heart disease death: acute pathological lesions

BACKGROUND: The majority of deaths due to acute coronary heart disease (CHD) occur outside hospital, unexpectedly, within the first few hours following the onset of the terminal event. Data on the incidence and nature of acute pathological findings in the affected hearts as seen in routine autopsies are somewhat controversial. Detailed pathological examination of coronary arteries and myocardium of such decedents was performed to clarify the situation. METHODS AND RESULTS: Full autopsy and detailed macroscopic and microscopic examination of the coronary arteries and myocardium were performed in 170 men, all registered in the Kaunas Acute Myocardial Infarct Register, who died outside hospital of CHD within 6 hours from the onset of symptoms. Out-of-hospital coronary death was in all cases related to acute ischaemic myocardial lesions, either myocardial infarction (MI) in 92.9% of cases or patchy micronecrosis in 7.1%. In the former group, the following stages of acute infarction were found: early MI (hyperacute phase) in 48.8% of cases, definite MI (displaying grossly identifiable coagulative necrosis) in 21.8% and progressing MI (presence of signs of early MI adjacent to a healing infarction) in 22.3%. Signs of new thrombotic coronary events were found in relation to these acute ischaemic myocardial lesions in 88.8% of cases, as occlusive thrombus in 41.2%, non-occlusive, mural thrombus in 37.0% and microthrombi/microemboli in intramyocardial vessels in 10.6%. CONCLUSIONS: Out-of-hospital coronary death most commanly was related to the early or definite stages of myocardial infarction. Accurate identification of these acute ischaemic lesions was based on detailed microscopic examination of the entire ventricular myocardium, with consideration being paid to signs of cardiomyocyte involvement and early inflammatory reaction associated with it. Acute pathology of the affected coronary artery usually confirmed that these myocardial infarct lesions were the cause of the sudden out of-hospital CHD-related deaths.     

Transient left ventricular ballooning (tako-tsubo cardiomyopathy) soon after intravenous ergonovine injection following caesarean delivery

Transient left ventricular ballooning also called tako-tsubo syndrome, is increasingly being recognized as cardiomyopathy mimicking the clinical scenario of an acute myocardial infarction. Generally, it is characterized by apical ballooning appearance of the left ventricle in the presence of normal coronary arteries on the angiogram. Recently, a variant form involving the midventricle with sparing of the apical and basal segments has been described. This syndrome is more prevalent in postmenopausal woman and usually preceded by extreme emotional and/or physical stress. We describe a case never reported before of transient left ventricular ballooning occurring during the early postpartum period after ergonovine injection rapidly evolving from a 'typical apical' ballooning into a 'midventricular' myocardial dysfunction.     

Acute myocardial infarction after simultaneous thrombosis in normal right and left coronary arteries

A 32-year-old male patient with clinical and electrocardiographic evidence of acute myocardial infarction underwent coronary angiographic study. We observed nonocclusive thrombosis simultaneously in right and left anterior descending coronary arteries, without confirmation of spasm or obstructive artery disease in other coronary branches. Documentation of coronary thrombosis in more than one artery is rare, and its pathophysiology is still unknown. With the advent of thrombolytic therapy and immediate coronary angiographic studies in patients with evolving myocardial infarction, it has been possible to confirm the presence of thrombus and the type of coronary disease. In this case, we observed total lysis of both thrombi and the final aspect of "normal" angiographically reperfused coronary arteries.     

The management of patients with acute myocardial infarction after successful reperfusion with streptokinase

Intracoronary streptokinase administration has been an effective procedure for establishing reperfusion of an evolving myocardial infarction by lysing the thrombus that is usually responsible for the infarction. After reperfusion is accomplished, appropriate management of the patient must be planned to provide the best chance for assuring continued vessel patency, and appropriate management of the patient's residual coronary artery disease also must be considered. In selected patients, percutaneous transluminal coronary angioplasty of the residual coronary lesion has been performed successfully immediately following reperfusion with streptokinase. Early coronary artery bypass graft surgery has been performed with good results in other patients. The appropriate management of the patient with acute myocardial infarction is still evolving, and only with additional study and experience will the "best" approach in the management of these patients be defined.     

Emergency myocardial revascularization in acute evolving myocardial infarct

Immediate coronary artery bypass for acute evolving myocardial infarction could be the elective therapy if provided on useful time, because myocardial salvage can be achieved by early reperfusion. Thirty eight patients had emergency coronary artery by-pass graft for acute evolving myocardial infarction during the early phase: 35 were male, the mean age was 51 years (34 to 74). The mean interval between the onset of symptoms and surgery in this series of patients was two hours and a half. This interval seems to be also the time limit in our experience to get a partial or complete recovery of ischemic area. Four patients died in hospital, but they were in severe cardiogenic shock before emergency surgery. Twenty nine cases were free of symptoms at a mean follow-up of 18 months (6 to 36) and two suffered for residual angina. Three patients died after discharge few months later: two during redo emergency vein grafts operations, one in deep left ventricular failure, while he was waiting for heart transplant. All these patients operated on as emergency developed acute myocardial infarction during their stay in hospital waiting for catheter study, surgical operation or during percutaneous transluminal coronary angioplasty. Saphenous vein grafts, were used in twenty nine patients, left internal mammary artery in nine cases, single in four and associated to saphenous vein in five, with an average number of anastomoses of 2.6 (1 to 6) for patient. ECG was found to be normal in 76% of the patients operated on within two hours and a half from the beginning of symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)     

Myocardial infarction in pregnancy associated with a coronary artery thrombus.

The case of a 36-year-old multigravid woman in whom acute myocardial infarction developed at five months post partum is described. Coronary angiography performed 11 days following myocardial infarction demonstrated a thrombus-like lesion in the coronary artery branch supplying the area of myocardial damage with no other evidence of coronary artery disease. This finding suggests that the development of a coronary artery thrombus is part of the mechanism of myocardial infarction in this case where the phenomenon of angiographically normal coronary arteries following myocardial infarction has bee- described. The mechanism leading to the development of a coronary thrombus in pregnancy is obscure, but may be similar to other clotting abnormalities complicating the third trimester and puerperium.     

Indications for coronary arteriography after myocardial infarction

The prognosis of patients after an acute myocardial infarction depends on the extent of the myocardial damage, its resulting left ventricular dysfunction and on the number and degree of narrowing of diseased coronary arteries. Patients with a severe multivessel disease constitute a high-risk group with an important morbidity and mortality during the first few months after hospitalization for a myocardial infarction. They could benefit from early revascularization therapy, whether by coronary artery bypass surgery, whether by percutaneous transluminal coronary angioplasty. Although early coronary revascularization is still controversial, management of patients after a myocardial infarction certainly will improve from a more accurate risk profiling by a careful diagnostic evaluation--including coronary arteriography in some subsets of patients--during the in-hospital period.     

Comparative efficacy of primary angioplasty with stent implantation and thrombolysis in restoring basal coronary artery flow in acute ST segment elevation myocardial infarction: quantitative assessment using the corrected TIMI frame count

Following thrombolysis and primary percutaneous transluminal coronary angioplasty (PTCA) for acute ST segment elevation myocardial infarction, basal flow in the culprit artery is known to influence prognosis. The purpose of this study was to determine if differences exist in basal flow in culprit and nonculprit coronary arteries in patients with acute ST segment elevation myocardial infarction who were treated with thrombolysis or primary PTCA with stent implantation. Twenty patients were randomized to thrombolysis (with recombinant tissue plasminogen activator) and 24 to primary PTCA with stent implantation within 3 hours of onset of acute ST segment elevation myocardial infarction. Coronary angiography was performed 90-120 minutes after thrombolysis or immediately after PTCA with stent implantation and again at 18-36 hours after intervention in both groups. Patients who failed to achieve thrombolysis in myocardial infarction (TIMI) grade 2 or 3 flow were excluded. The corrected TIMI frame count was used as the index of basal coronary artery flow. Early after intervention the mean corrected TIMI frame count in the culprit coronary artery was significantly lower in the primary PTCA with stent group (27.4 +/- 7.7 frames) than in the thrombolysis group (39.8 +/- 10 frames, p < 0.001). Eight thrombolysis patients (40%) and 20 primary PTCA patients (83%, p < 0.01) achieved TIMI grade 3 flow early after intervention. By 18-36 hours after intervention there were no significant differences in the mean correct TIMI frame count between the thrombolysis and primary PTCA with stent groups. There were no significant differences in the mean corrected TIMI frame count between these two groups in the nonculprit coronary artery, either early after intervention or at 18-36 hours. In successfully reperfused coronary arteries following acute ST segment elevation myocardial infarction, primary angioplasty with stent implantation reestablished TIMI grade 2 or 3 flow faster and more effectively than thrombolysis did.     

Possible role of coronary spasm in acute myocardial infarction precipitated by hyperventilation

Acute myocardial infarction was precipitated by hyperventilation in a 65 year old man. His coronary arteriogram in the chronic phase showed almost normal coronary arteries. Injection of acetylcholine (50 micrograms) into the left coronary artery induced spasm of the circumflex artery with chest pain in association with ST-segment elevation in the inferior leads and ST-segment depression in the precordial leads. In this patient there may have been atherosclerosis of the coronary arteries with absent or dysfunctional endothelium, despite an almost normal angiographic appearance. In the absence of endothelium the response of the smooth muscle to acetylcholine is constriction.     

Possible role of coronary spasm in acute myocardial infarction precipitated by hyperventilation.

Acute myocardial infarction was precipitated by hyperventilation in a 65 year old man. His coronary arteriogram in the chronic phase showed almost normal coronary arteries. Injection of acetylcholine (50 micrograms) into the left coronary artery induced spasm of the circumflex artery with chest pain in association with ST-segment elevation in the inferior leads and ST-segment depression in the precordial leads. In this patient there may have been atherosclerosis of the coronary arteries with absent or dysfunctional endothelium, despite an almost normal angiographic appearance. In the absence of endothelium the response of the smooth muscle to acetylcholine is constriction.     

Specific platelet mediators and unstable coronary artery lesions. Experimental evidence and potential clinical implications

We have speculated previously that the abrupt conversion from chronic stable to unstable angina and the continuum to acute myocardial infarction may result from myocardial ischemia caused by progressive platelet aggregation and dynamic vasoconstriction themselves caused by local increases in thromboxane and serotonin at sites of coronary artery stenosis and endothelial injury. Platelet aggregation and dynamic coronary artery vasoconstriction probably result from the local accumulation of thromboxane and serotonin and also relative decreases in the local concentrations of endothelially derived vasodilators and inhibitors of platelet aggregation, such as endothelium-derived relaxing factor (EDRF) and prostacyclin. With severe reductions in coronary blood flow caused by these mechanisms, platelet aggregates may increase, and an occlusive thrombus composed of platelets and white and red blood cells in a fibrin mesh may develop. When coronary arteries are occluded or narrowed for a sufficient period of time by these mechanisms, myocardial necrosis, electrical instability, or sudden death may occur. We believe that unstable angina and acute myocardial infarction are a continuum in relation to the process of coronary artery thrombosis and vasoconstriction. When the period of platelet aggregation or dynamic vasoconstriction at sites of endothelial injury and coronary artery stenosis is brief, unstable angina or non-Q wave infarction may occur. However, when the coronary artery obstruction by these mechanisms is prolonged for several hours, Q wave myocardial infarction results. Chronic endothelial injury and coronary artery stenosis are probably associated with the accumulation of platelets, white and red blood cells, and a fibrin mesh at the site of stenosis and endothelial injury.     

The heart in fatal unstable angina pectoris

Compared to patients with sudden coronary death and acute myocardial infarction, relatively little morphologic data has been reported in patients with unstable angina pectoris. This article reviews necropsy data collected from one laboratory on unstable angina pectoris. From these data, several observations are appropriate: (1) Patients with unstable angina as a group have more coronary narrowing by atherosclerotic plaque than do patients with sudden coronary death or acute or healed myocardial infarction. (2) Patients with unstable angina have a much higher frequency of severe narrowing of the left main coronary artery than do patients in other coronary subsets. (3) The coronary atherosclerotic plaques in unstable angina consist primarily of fibrous tissue, and they are more similar to those found in patients with sudden coronary death than in patients with acute myocardial infarction. (4) The frequency of acute coronary lesions (thrombi, plaque rupture, and plaque hemorrhage) is similar to that observed in patients with sudden coronary death and significantly less than that observed in acute myocardial infarction. (5) The frequency of multiluminal channels throughout the major coronary arteries is significantly higher in unstable angina compared to sudden coronary death or acute myocardial infarction. (6) The major epicardial arteries and the heart are smaller in patients with unstable angina than in patients with sudden coronary death or acute myocardial infarction. (7) The left ventricular cavity is usually of normal size in patients with unstable angina and therefore left ventricular function is usually normal.     

心肌缺血再灌注损伤机制研究的回顾与展望

心肌梗死是全球冠心病患者死亡的主要原因之一。在急性心肌梗死早期行经皮冠状动脉介入术、冠状动脉旁路移植术、药物等治疗手段,可恢复缺血区心肌组织血供,挽救濒死的心肌,降低患者的致死率。然而,心肌血供中断后,一定时间内再通恢复血供后,原缺血心肌可发生较缺血时更为严重的损伤,这一现象称为心肌缺血再灌注损伤(MIRI),其发生机制尚未完全阐明。文章就近年来MIRI机制的研究进展作一综述,阐述MIRI的病理生理机制,将有助于开发新的治疗干预手段,为临床治疗心肌梗死提供帮助。