ObjectivesThe present study attempts to identify appropriate elements that may contribute to clarify the broad clinical features (diagnosis, care, complication and prognosis) of Takotsubo-like cardiomyopathy for improving its management.Design studyObservational study.SettingPrimary level of care referred to the emergency department of Vannini Hospital, Rome, Italy.ParticipantsThe study population consisted of 75 patients, 72 of the them were women and 3 were men with a mean age of 71.9±9.6 years.MethodsFrom February 2004 to November 2010, prospectively included 84 consecutive patients diagnosed for suspected Takotsubo-like cardiomyopathy. To be eligible, patients had to meet all the Mayo clinic criteria in the absence of neurological trauma or intracranial haemorrhage. Moreover, those patients that at follow-up still presented alteration of acute phase at ECG and echocardiogram were excluded. Thus, 75 patients comprised the study population. To follow-up 19 patients were lost.ResultsNone of 75 patients died in acute phase. All patients were promptly discharged (8.4±4.4 days), since they recovered their normal functional status without symptoms. Follow-up information was available for 56 patients. At a mean follow-up time of 2.2±2 years (range, 0.1–6.8 years) two octogenarian patients (2.6%) died because of sudden cardiac death and pulmonary embolism, respectively. The Takotsubo-like cardiomyopathy recurred in one patient.ConclusionsThe results of this study support the previous reports about the good prognosis, also in critically ill patients, of Takotsubo-like cardiomyopathy. Further assessment will be needed to determine a careful and sustained follow-up for choosing the best care and foreseeing the recurrences of this emerging condition.

Stress cardiomyopathy is a reversible left ventricular dysfunction triggered by emotional stress. We describe a variant of transient left ventricular ballooning in a patient in which basal and midventricular segments are affected. This confirms that there is not just one ventricular dysfunction pattern in Takotsubo cardiomyopathy. The involvement of only the basal and midventricle segments is an intriguing observation with no clear explanation; furthermore, there are no predictive factors for the differently sited wall motion abnormalities.

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Hypertrophic cardiomyopathy is a disease of the myocardium characterized by the thickening of the heart walls. It is a genetic disorder transmitted by first-degree relatives, caused by mutations in genes that code for sarcomere protein.A 77-year-old woman presented to the emergency department and complained of continuous vertigos and presyncope with subsequent fall to the floor with a concussive traumatic brain injury. The ECG observed signs of left ventricular hypertrophy. Blood exams highlighted a slight increase of troponin T (25 ng/L). The ultrosonography instead demonstrated a pronounced left ventricular hypertrophy with a 240 mmHg dynamic gradient, a moderate mitral regurgitation secondary to SAM.Lastly, ECG Holter excluded significant arrhythmias (1 couple of ventricular contractions). In the ward, the echocardiographic pattern was repeated and confirmed the clinical picture of a pronounced ventricular hypertrophy at the expense of the IVS (VTD 45 ml), a diastolic dysfunction Grade I with anterior systolic movement of the mitral flap valves with a dynamic obstruction to the left ventricular outflow (DP max 260 mmHg). Moreover, a moderatesevere mitral insufficiency was reported. Vital signs were stable.The antihypertensive therapy was enhanced with added ACE inhibitors, loop diuretics, beta blockers and the disopyramide administration started. The patient was discharged from the hospital and was scheduled a cardiologic echocardiographic follow up in order to evaluate the effectiveness of the therapy. This study has demonstrated the association between the clinical symptom, the clinical objectivity and the echocardiographic anomalies typical of the obstructive hypertrophic cardiomyopathy. Severe blood pressure values of dynamic obstruction to the left ventricular outflow have been recorded and which are not currently known by the scientific literature. Our purpose will be to evaluate the clinical and echocardiographic follow up and the potential response to the pharmacological therapy prescribed.

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