Overview
An old infarct of the myocardium in the posterolateral region represents a chronic condition resulting from a previous ischemic insult to the heart muscle. This type of myocardial infarction (MI) often leads to significant structural and functional changes within the affected area and the surrounding myocardium. The posterolateral region, encompassing parts of the lateral wall of the left ventricle, is particularly vulnerable due to its unique coronary artery supply. Over time, the healing process following an infarct can result in scar tissue formation, which not only compromises local contractility but also affects global cardiac function and predisposes the patient to various complications such as arrhythmias and heart failure. Understanding the pathophysiology, clinical presentation, and management strategies for this condition is crucial for optimizing patient outcomes.
Pathophysiology
The pathophysiology of an old infarct in the posterolateral region involves complex alterations in myocardial structure and function. Reduced density of inward calcium currents (ICa) observed in both the remote myocardium (REM) and the infarct region (MI) plays a pivotal role in these changes [PMID:9160231]. In the infarct region, the decrease in ICa density likely reflects structural modifications to calcium channels, possibly due to cellular damage and subsequent repair mechanisms that may not fully restore normal channel function. This alteration can impair calcium handling, a critical process for muscle contraction and relaxation, leading to impaired contractility and potential arrhythmias.
In the remote myocardium, reduced ICa density might indicate compensatory hypertrophy or adaptive changes aimed at maintaining cardiac output in the face of reduced functional myocardium. These adaptive mechanisms, while initially beneficial, can also predispose the heart to further dysfunction if they exacerbate metabolic demands or disrupt normal electrical conduction pathways. The interplay between these regions—where the viable myocardium attempts to compensate for the infarcted area—highlights the systemic impact of localized damage on overall cardiac performance. This complex interplay underscores the importance of considering both the infarcted and remote myocardial regions in the clinical management of these patients.
Clinical Presentation
Patients with an old infarct in the posterolateral region often present with a constellation of symptoms reflecting both the direct consequences of myocardial damage and compensatory mechanisms in the surrounding myocardium. Significant alterations in calcium currents observed in both the infarct and remote myocardium can underlie persistent clinical manifestations such as arrhythmias, decreased cardiac efficiency, and symptoms of heart failure [PMID:9160231]. Arrhythmias, particularly ventricular tachycardia and fibrillation, are common due to the re-entry circuits facilitated by scar tissue and altered electrical conduction pathways. These arrhythmias can be life-threatening and require vigilant monitoring and management.
Decreased cardiac efficiency manifests clinically as dyspnea, fatigue, and exercise intolerance, reflecting the compromised ability of the heart to pump blood effectively. The posterolateral location of the infarct can specifically affect left ventricular function, impacting ejection fraction and overall cardiac output. Additionally, patients may experience angina pectoris, especially during physical exertion, as the remaining viable myocardium struggles to meet increased metabolic demands. In clinical practice, these symptoms often necessitate a thorough evaluation including echocardiography, electrocardiography (ECG), and possibly cardiac MRI to assess the extent of scarring and functional impairment accurately.
Diagnosis
Diagnosing an old infarct in the posterolateral region involves a multifaceted approach aimed at confirming the presence of scar tissue and assessing its impact on cardiac function. Electrocardiography (ECG) remains a foundational tool, often showing nonspecific changes such as T-wave inversions or left bundle branch block patterns, especially in the acute phase. However, in chronic cases, the ECG may appear relatively normal or show only subtle signs of previous infarction. Echocardiography is crucial for visualizing wall motion abnormalities and estimating ejection fraction, providing insights into the functional impact of the infarct.
Cardiac MRI (CMR) offers superior sensitivity and specificity for detecting myocardial scarring and delineating the extent of the infarct. CMR can differentiate between viable and non-viable myocardium, which is invaluable for understanding the patient's prognosis and guiding therapeutic decisions. Additionally, late gadolinium enhancement (LGE) imaging during CMR is particularly useful for identifying areas of fibrosis characteristic of old infarcts. Biomarker analysis, including troponin levels, though typically elevated acutely, can help rule out ongoing myocardial injury in the context of chronic presentations. In clinical practice, integrating these diagnostic modalities provides a comprehensive assessment of the patient's condition, facilitating tailored management strategies.
Management
The management of patients with an old infarct in the posterolateral region focuses on mitigating symptoms, preventing complications, and improving overall cardiac function. Given the evidence of reduced ICa density and altered calcium channel properties in both the infarct and remote myocardium [PMID:9160231], therapeutic strategies targeting calcium channel modulation emerge as a promising avenue. Calcium channel blockers, such as verapamil or diltiazem, may be considered to stabilize cardiac electrical activity and reduce the risk of arrhythmias by modulating calcium influx and outflow. However, their use should be carefully balanced against potential negative inotropic effects, particularly in patients with compromised cardiac function.
Lifestyle modifications are foundational, emphasizing smoking cessation, dietary changes to reduce cholesterol and sodium intake, and regular physical activity tailored to the patient's functional capacity. Pharmacological management often includes beta-blockers to improve survival and reduce the risk of recurrent ischemic events, as well as ACE inhibitors or angiotensin receptor blockers (ARBs) to enhance cardiac remodeling and reduce afterload. Diuretics may be necessary to manage fluid overload and alleviate symptoms of heart failure.
In cases where heart failure symptoms are refractory to medical therapy, advanced interventions such as cardiac resynchronization therapy (CRT) or implantable cardioverter-defibrillators (ICDs) might be considered, especially if there is evidence of conduction abnormalities or a high risk of sudden cardiac death. Regular follow-up with echocardiography and clinical assessment is essential to monitor disease progression and adjust treatment as needed. This comprehensive approach aims to optimize cardiac function, manage symptoms effectively, and reduce the risk of adverse outcomes in patients with old posterolateral myocardial infarcts.
Key Recommendations
References
1 Pinto JM, Yuan F, Wasserlauf BJ, Bassett AL, Myerburg RJ. Regional gradation of L-type calcium currents in the feline heart with a healed myocardial infarct. Journal of cardiovascular electrophysiology 1997. link
1 papers cited of 3 indexed.