· neurogenic myocardial stunning,
· stress cardiomyopathy
· stress-induced cardiomyopathy,
· transient left ventricular apical ballooning,
· "ampulla" cardiomyopathy
· Tako-tsubo syndrome
Broken heart Syndrome is an increasingly reported syndrome characteriz
ed by transient apical or midventricular left ventricular dysfunction that mimics myocardial infarction (MI), but in the absence of significant coronary artery disease.
CLINICAL PRESENTATION — The clinical presentation of stress-induced cardiomyopathy is similar to that of an acute MI, usually with ST elevation . The most common presenting symptom is acute substernal chest pain, but some patients present with dyspnea, shock, or electrocardiographic abnormalities.
The range of findings from these reports is illustrated by the following:
Electrocardiographic abnormalities are the most common finding. ST segment elevation was present in 82 percent of patients (208 of 255) in the systematic review. Among these patients, ST elevations were most common in the anterior precordial leads (82 percent or 172 of 205 patients). Additional ECG abnormalities have also been described, including ST segment depression, T wave inversion, QT interval prolongation, and abnormal Q waves are also seen in some patients.
Cardiac biomarkers are frequently elevated. However, the enzyme elevations are typically mild, which is inconsistent with the often severe hemodynamic compromise. In the systematic review, among studies that measured cardiac troponins or creatine kinase MB, these levels were elevated in 86 and 74 percent of patients, respectively.
Left ventriculography or echocardiography usually show the characteristic apical ballooning with akinesis or dyskinesis of the apical one-half to two-thirds of the LV . Overall systolic function is reduced, and the reported average LVEF has ranged from 20 to 49 percent. In separate reports of ten other cases, ballooning has involved the middle or basal portions of the left ventricle but not the apical segment . No obvious mechanism for this difference in location has been identified.
In the systematic review, transient LVOT obstruction was reported in 16 percent of the patients (21 of 133) who underwent left ventriculography. In some cases, this is accompanied by systolic anterior motion of the mitral valve, similar to that seen in hypertrophic cardiomyopathy.
Reversible perfusion abnormalities in the left ventricular apex have been documented, while
magnetic resonance imaging typically shows mid and apical LV segmental wall motion abnormalities, often in multiple coronary territories without delayed hyperenhancement of involved regions.
Diagnosis — The diagnosis of stress-induced cardiomyopathy should be suspected in postmenopausal women who present with an acute coronary syndrome after intense psychologic stress in whom the clinical manifestations and ECG abnormalities are out of proportion to the degree of elevation in cardiac enzymes.
ECG1
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ECG3
Left ventricular apical ballooning or midventricular hypokinesis is usually seen on left ventriculography or echocardiography. In a minority of cases (40 percent in one report), transient left ventricular hypokinesis is midventricular ("atypical") rather than apical ("typical) .
Coronary angiography, by definition, reveals no critical coronary lesions. However, in addition to stress-induced cardiomyopathy, a number of other syndromes have been associated with ST segment changes in the absence of significant coronary artery disease, including cardiac syndrome X, variant (Prinzmetal's) angina, and cocaine abuse.
The systematic review cited above proposed the following four diagnostic criteria, all of which must be met :
1- Transient akinesis or dyskinesis of the apical and midventricular segments in association with regional wall motion abnormalities that extend beyond the distribution of a single epicardial vessel
2- Absence on angiography of obstructive coronary artery disease or evidence of acute plaque rupture
3- New ST segment elevation or T wave inversion on the ECG
4- Absence of recent significant head trauma, intracranial bleeding, pheochromocytoma , myocarditis, or hypertrophic cardiomyopathy .
There are no standard treatment guidelines for treating broken heart syndrome. Treatment is similar to treatment for a heart attack until the diagnosis is clear. Most people stay in the hospital while they recover.
Once it's clear that broken heart syndrome is the cause of your symptoms, your doctor will likely prescribe heart medications for you to take while you're in the hospital, such as angiotensin-converting enzyme (ACE) inhibitors, beta blockers or diuretics. These medications help reduce the workload on your heart while you recover and may help prevent further attacks. Many patients make a full recovery within one to two months.
Procedures that are often used to treat a heart attack, such as balloon angioplasty and stent placement, or even surgery, are not helpful in treating broken heart syndrome. These procedures treat blocked arteries, which are not the cause of broken heart syndrome. However, coronary angiography is often used to diagnose exactly what's the cause of the chest pain.
