Transient Left Ventricular Dysfunction from Cardiomyopathies to Myocardial Viability: When and Why Cardiac Function Recovers

Abstract

Transient left ventricular dysfunction (TLVD), a temporary condition marked by reversible impairment of ventricular function, remains an underdiagnosed yet significant contributor to morbidity and mortality in clinical practice. Unlike the well-explored atherosclerotic disease of the epicardial coronary arteries, the diverse etiologies of TLVD require greater attention for proper diagnosis and management. The spectrum of disorders associated with TLVD includes stress-induced cardiomyopathy, central nervous system injuries, histaminergic syndromes, various inflammatory diseases, pregnancy-related conditions, and genetically determined syndromes. Furthermore, myocardial infarction with non-obstructive coronary arteries (MINOCA) origins such as coronary artery spasm, coronary thromboembolism, and spontaneous coronary artery dissection (SCAD) may also manifest as TLVD, eventually showing recovery. This review highlights the range of ischemic and non-ischemic clinical situations that lead to TLVD, gathering conditions like Tako-Tsubo Syndrome (TTS), Kounis syndrome (KS), Myocarditis, Peripartum Cardiomyopathy (PPCM), and Tachycardia-induced cardiomyopathy (TIC). Differentiation amongst these causes is crucial, as they involve distinct clinical, instrumental, and genetic predictors that bode different outcomes and recovery potential for left ventricular function. The purpose of this review is to improve everyday clinical approaches to treating these diseases by providing an extensive survey of conditions linked with TLVD and the elements impacting prognosis and outcomes.

Keywords: MINOCA; Tako-Tsubo Syndrome (TTS); cardiomyopathies; left ventricular function recovery; transient left ventricular dysfunction; viability.

Figure 1

Summary of the main pathogenetic mechanisms of transient left ventricular dysfunction. CM, Cardiomyopathy; S, Syndrome.

Figure 2

Examples of stunned and hibernated myocardium. (a) Aborted AMI treated with PTCA and stent implantation in LAD—WMA 3 in anterior septum and no LGEi. (b) Anteroseptal AMI small area of LGEi (red arrow) associated with a diffuse hyperintensity on T2w-STIR images associated with WMA 3. (c) Severe LV dysfunction (EF 38%) in absence of LGE and T2w-STIR. (d) WMA 3 in anterolateral and inferolateral wall with LGE > 50% and no area of hyperintensity on T2w-STIR. Abbreviations. AMI: acute myocardial infarction; EF: ejection fraction; LAD: left anterior descending artery; LGEi: late gadolinium enhancement imaging; LV: left ventricle; T2w-STIR: T2 weighted short tau inversion recovery; WMA: wall motion abnormality.

Figure 3

Schematic representation of myocardial responses to left ventricular dysfunction.