Post-infarction angina: mechanisms of development, clinical features, treatment, and prognosis - Bobrov V. O. 2009

Clinical observation of patients with post-infarction angina

The impact of the course of acute myocardial infarction (AMI) on the formation and development of post-infarction myocardial ischemia (PIMI). Early post-infarction angina is the single most prognostic-worsening syndrome in the clinical course of myocardial infarction, leading to fatal and non-fatal myocardial infarction, reinfarction, and sudden cardiac death. Therefore, this issue is of paramount importance and warrants more detailed investigation.

To analyze the impact of the acute phase of myocardial infarction on The Development of post-infarction myocardial ischemia in patients with myocardial infarction, 358 patients presenting with primary acute myocardial infarction (mean age 54.2±7.3 years) were examined. The Diagnosis of the underlying condition was established based on clinical findings, General clinical examination, and specialized laboratory and instrumental Methods. All patients received standard conventional therapy. On days 7–9 following the onset of acute myocardial infarction, all patients underwent 24-hour Holter ECG monitoring using a DRG Holter Reporter device (USA), which records ECGs across three modified leads. The inferior orthogonal "y" lead and transthoracic V2 and V9R leads were utilized. The following Holter ECG parameters were evaluated:

a) ST-segment dynamics duration (ST min);

b) frequency of ischemic episodes (ST ep.);

c) magnitude of ST-segment depression (STdep.);

d) duration of the maximum ST segment (ST max).

Throughout the study, patients kept a detailed diary of all their symptoms, paying particular attention to episodes of angina pectoris.

At the initial stage of the study, all patients were divided into two groups: the first (control) group comprised patients without detected early post-infarction angina (EPA) (with ST-segment depression of less than 1 mm or no depression according to Holter data), and the second group comprised patients with detected EPA (with ST-segment depression exceeding 1 mm according to Holter data).

The percentage distribution of patients across the groups was as follows: 226 patients (63.1%) without EPA, and 132 patients (36.9%) with EPA. Essential Hypertension was more prevalent among patients with EPA, although this difference was not statistically significant (52.2% versus 43.4% and 42.5%). The duration of hypertension did not differ between the patient groups. Previous studies similarly found no significant difference between groups regarding a history of hypertension.

Stage I–IIA Heart Failure was observed more frequently in patients with EPA compared to the control group (62.5% and 63% versus 47.3%; p>0.05).

The most influential factors contributing to the development of EPA in the post-infarction period During the first days following AMI included the duration of coronary artery disease (CAD) prior to the onset of MI, the duration of pre-infarction angina, and the presence of hypertension and heart failure. Our findings are consistent with those of several other authors. Specifically, the development of collateral vessels during the course of CAD helped protect the myocardium against EPA, whereas prolonged unstable pre-infarction angina promoted the development of EPA. The Role of a history of hypertension in the development of EPA remains a subject of debate. A trend toward promoting EPA—both silent ischemia and EPA in patients with Stage I–IIA heart failure—was observed.

During an 18-month follow-up period, the impact of events occurring during the first hours and days on the clinical course and prognosis of myocardial infarction became evident. Specifically, the presence of acute left ventricular failure (ALVF), ventricular fibrillation, intraventricular and atrioventricular conduction disturbances, and ventricular tachycardia within the first days of AMI development all contributed to the development of EPA in myocardial infarction patients.

We also examined METABOLISM/18.html">The Influence of events during the first days of the post-infarction period on the prognosis of patients with and without EPA. Clinical endpoint data were evaluated 18 months after the onset of AMI (Table 1).

Table 1. The impact of rhythm and conduction disturbances in myocardial infarction patients on the development of reinfarction and death within 18 months post-AMI

As shown in Table 1, the presence of myocardial electrical instability and conduction disturbances during the acute phase of myocardial infarction represents a highly significant risk factor for cardiac death in the post-infarction period, regardless of whether patients present with or without post-infarction ischemia. Notably, the occurrence of reinfarction did not depend on these factors.

Thus, patients in whom EPA was detected had a history of coronary artery disease exceeding one year. The duration of pre-infarction angina was longest in patients with EPA. The presence of acute left ventricular failure during the first week of AMI promotes the development of EPA. Intraventricular and atrioventricular conduction disturbances, as well as life-threatening arrhythmias such as ventricular tachycardia and ventricular fibrillation, occurred nearly 4 times more frequently in patients with EPA. During long-term follow-up, myocardial electrical instability and conduction disturbances during the acute phase of MI proved to be critical risk factors for cardiac death in the post-infarction period for patients both with and without post-infarction ischemia. The development of reinfarction was independent of this cause.

The influence of AMI Treatment modalities on the development of post-infarction myocardial ischemia. According to the guidelines of the American Heart Association for reducing cardiovascular mortality in patients with CAD and atherosclerosis, as well as the European Society of Cardiology in collaboration with the European Societies for the Prevention of Atherosclerosis and Arterial Hypertension, patients with AMI require comprehensive medical therapy, including antithrombotic therapy, beta-blockers, and ACE inhibitors. The administration of long-acting nitrates and calcium channel antagonists in individually adjusted doses also remains highly relevant. In recent years, several large-scale trials have highlighted the role of thrombolytic therapy or percutaneous transluminal coronary angioplasty (PTCA) in the management of AMI. However, the question of how various treatment modalities for AMI affect the clinical course, the development of EPA subtypes, and adverse prognosis remains open.

To analyze the efficacy of AMI treatment modalities and their impact on the subsequent development of EPA, 358 patients with primary AMI were evaluated. All patients received standard conventional therapy. Patients hospitalized within 6 hours of symptom onset and lacking contraindications underwent thrombolytic therapy with kabikinase at the following dosages: intravenous administration of 1,500 thousand IU, and intracoronary administration of 750 thousand IU. Intracoronary thrombolytic therapy was performed at the Department of Hospital Surgery of the Zaporizhzhia Medical Institute (cardiosurgical and intravascular radiology department of the Zaporizhzhia Regional Clinical Hospital).

Among the patients who underwent thrombolytic therapy, 14 (35%) developed silent myocardial infarction (SMI), and 21 (22.8%) developed EPA.

As demonstrated in Table 2, all patients received standard treatment, though minor differences in medication usage were observed between the groups. It should be emphasized that the efficacy of medical therapy plays a crucial role from the very first hours of AMI. Therefore, patients who showed an inadequate response to heparinization, beta-blockers, and ACE inhibitors were prescribed nitrates. A comparative Analysis of the effects of medical therapy and thrombolytic therapy on the development of post-infarction myocardial ischemia in AMI patients is presented in Table 3.

Specifically, following medical therapy alone, EPA did not develop in 133 (58.8%) patients, whereas after intravenous thrombolytic therapy, it was avoided in 56 (63.8%) patients. Following intracoronary thrombolytic therapy, 87.5% of patients also did not develop EPA.

Table 2. Types of treatment administered in the studied patient groups

Table 3. Comparative analysis of the efficacy of thrombolytic therapy versus medical treatment in patients with AMI

*p<0,05 compared with the group of patients who underwent intracoronary thrombolytic therapy

During the 18-month follow-up of patients with AMI, we analyzed the efficacy of the administered treatment and, consequently, its impact on the development of study endpoints—reinfarction and death (Table 4).

As shown in Table 4, among patients who received medical therapy alone, reinfarction developed in 19,4 % of patients with RMI, compared to 8,3 % in those who received timely systemic thrombolysis, whereas no cases of reinfarction were observed following timely intracoronary thrombolysis. There were no deaths among patients with RMI who underwent intravenous or intracoronary thrombolysis, while medical therapy alone resulted in a mortality rate of 8,4 %.

Among patients without myocardial ischemia who received medical therapy alone, reinfarction occurred in 9,8 %, compared to 3,6 % after intravenous thrombolytic therapy. No cases of reinfarction were observed in patients without myocardial ischemia who underwent intracoronary thrombolysis. Deaths in this patient group occurred exclusively with medical therapy.

The question of comparing the efficacy of intracoronary versus intravenous thrombolysis in AMI remains a subject of debate; however, some authors note that intracoronary thrombolysis achieves higher rates of coronary artery recanalization using lower doses of kabikinase, while reducing complications and mortality.

Table 4. Comparative analysis of treatment efficacy in patients with AMI over an 18-month period

Thus, the analysis of the incidence of study endpoints—reinfarction and death—depending on the administered treatment leads to the Conclusion that intracoronary thrombolysis and PTCA are the most effective methods for treating AMI. The development of silent myocardial ischemia (SMI) or RMI depends on the procedural success of PTCA. A residual stenosis of 75–90 % contributes to the development of RMI.

Medical therapy is the most widespread and accessible method for preventing RMI. Timely and rational administration of heparinization, beta-blockers, and ACE inhibitors helps protect the myocardium against post-infarction ischemia.

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