In this case, Echocardiography has to be Interpreted in the CONTEXT of clinical findings.

Conditions like Anemia[Chronic TARCHICARDIA], Hypothyrodism, & hAEMOCHROMATOSIS  have to be investigated[NO pathognomic features on ECHO]

Though clinical context is very important, absence of scarring and thining of LV wall, relatively less dilatation of cardiac chambers and apical ballooning may be indirect indicator.Thanks Asad for ur answar. 

This may ne very difficult as there are very few pathognomonic features of reversible cardiomyopathy on echocardiography. Most are basically suggestive. Apart from that many other causes of cardiomyopathy may be structural such as microsomal, ribosomal etc. Many heart diseases appear similar in advances heart failure on echocardiography and even biopsy may not be as helpful as in early stages.

Obesity, tachycardia, and extreme stress have all been shown to result in impaired left ventricular function and dilatation. Several of these reversible CMs, including:

• Tachycardia-induced (ECG and ECHO: arrhythmias include atrial fibrillation, atrial flutter, atrial tachycardia, reentrant supraventricular tachycardia, accessory pathway tachycardia, frequent ectopic beats, and ventricular tachycardia. Persistent tachycardia causes elevated ventricular filling pressures, severe biventricular systolic dysfunction, reduced cardiac output, and elevated systemic vascular resistance)
• Takotsubo (contractile function of the mid and apical segments of the LV are depressed and there is hyperkinesis of the basal walls, producing a balloon-like appearance of the distal ventricle with systole)
• Sepsis-induced cardiomyopathy (Increased LVEDP is indicative of diastolic dysfunction in sepsis patients),
• Thyroid Disease–Induced Cardiomyopathy (systemic changes in cardiac function due to reduced peripheral vascular resistance, activation of the renin–angiotensin mechanism, increased LV end-diastolic volume (LVEDV) and increased preload; the increased preload and decreased peripheral vascular resistance leads to a high cardiac output, even at rest, resulting in CM. In contrast to hyperthyroidism, hypothyroidism causes a low cardiac output CM via the same pathways mentioned above, however, by downregulating the previously mentioned receptors/channels causing decreased myocardial excitation and contractility leading to a low-output CM)
• Peripartum CM (by clinical criteria: ( development of heart failure symptoms either during the last month of pregnancy or within the first 5 months after delivery;  no other identifiable causes of HF exist; no evidence of heart disease prior to the last month of pregnancy)
• Inflammatory CM (there are both non-infectious and infectious causes . Non- infectious origins include toxins, alcohol, cytotoxic chemotherapy, and metabolic abnormalities)