Quantitative autoradiographic delineation of the distribution of beta-adrenergic receptors in canine and feline left ventricular myocardium.

193

131

akotsubo-like left ventricular (LV) dysfunction ischaracterized by a unique morphologic feature on left ventriculography (LVG) and some clinical features, including a predominance in elderly women, as well as a favorable prognosis. [1][2][3][4][5][6][7][8][9] The LV wall motion abnormality is quite different from that in myocardial infarction; it occurs in the LV apical region (LV apical ballooning), but improves within several weeks. The precise mechanism remains still unclear. Kurisu et al reported that coronary microcirculation, assessed by thrombolysis in myocardial infarction trial frame count, is impaired in patients with takotsubo-like LV dysfunction. 4 And Nishikawa et al reported that coronary microvascular function assessed by 99m Tc-tetrofosmin myocardial single photon emission computed tomography is impaired in patients with takotsubo-like LV dysfunction. 6 It has been also reported that the coronary flow velocity (CFV) pattern and CFV reserve (CFVR), measured with a Doppler guidewire, reflect the degree of coronary microvascular dysfunction under stable hemodynamic conditions in the absence of epicardial coronary stenosis, 10-14 so the aim of the present study was to evaluate coronary microcirculation in patients with takotsubo-like LV dysfunction by analyzing CFV pattern and CFVR in the acute phase and 3 weeks later. Methods Study PatientsWe studied 8 consecutive patients with takotsubo-like LV dysfunction (7 females, 1 male). All patients were diagnosed with takotsubo-like LV dysfunction according to the following criteria: (1) LV wall motion abnormality mainly at the apex on LVG; (2) ST-segment elevation or T-wave abnormality in at least 2 contiguous electrocardiogram (ECG) leads; (3) no history of prior myocardial infarction; and (4) normal coronary angiography (CAG) (luminal narrowing of <25% in all 3 coronary arteries). We excluded patients with subarachnoid hemorrhage, pheochromocytoma crisis, atrial fibrillation, hypertrophic cardiomyopathy, severe valvular heart disease and post-tachycardia condition. The existence of hypertension, hyperlipidemia, diabetes mellitus, and smoking were determined, using the following criteria: hypertension was defined as blood pressure >140/90 mmHg or current medication; hyperlipidemia was defined as total cholesterol concentration >220 mg/dl, triglyceride concentration >150 mg/dl or current medication; diabetes mellitus was defined as fasting plasma glucose concentration >120 mg/dl, plasma glucose concentration (anytime) >200 mg/dl or current medication. Within 24 h of symptom onset, LVG and CAG were performed by the femoral approach after intravenous infusion of 5,000 U of heparin. LV end-diastolic pressure (LVEDP) was obtained before LVG. After confirming the LV apical wall motion abnormality and normal CAG, the phasic CFV spectrum was recorded at rest and during hyperemia induced by an intravenous injection of 0.15 mg·kg -1 ·min -1 adenosine 5'-triphosphate, in the middle portion of the left anterior descending coronary artery (LAD), the left circumflex ar...

Section: Discussionmentioning

confidence: 44%

Assessment of Coronary Microcirculation in Patients With Takotsubo-Like Left Ventricular Dysfunction

Kume

Akasaka

Kawamoto

et al. 2005

193

131

“…One possible explanation is the different distribution of sympathetic nerves and the density of receptors in the LV myocardium (ie, being high in basal segments and low in the apex for the nerves, and low in basal segments and high in the apex for the receptors). 15,16 We speculate that the distribution of sympathetic receptors corresponds to the distribution of the pathological changes in the present patient, which in turn corresponds to contraction abnormalities of the left ventricle. In an animal study, a 180-min electrical stimulation of a unilateral dorsal medulla in vagotomized cats caused significant dilatation of the left ventricle, especially in the apex, and additionally cardiac pathology revealed contraction band necrosis, myocardial hemorrhage and cardiomyocyte apoptosis.…”

Section: Discussionmentioning

confidence: 55%

Left Ventricular Apical Rupture Caused by Takotsubo Cardiomyopathy - Comprehensive Pathological Heart Investigation

Sacha¹,

Maselko²,

Wester³

et al. 2007

akotsubo cardiomyopathy is a novel heart syndrome characterized by a transient left ventricular (LV) dysfunction with chest pain, ECG changes and not a high increase in cardiac enzymes, mimicking an acute myocardial infarction. 1,2 Because of the specific abnormalities of the LV contraction (ie, preserved basal function with apical akinesis or dyskinesis) the disease is also called as 'transient left ventricular apical ballooning' or 'ampulla cardiomyopathy '. 2,3 The general prognosis is considered to be rather favorable, 2-6 although some investigators have reported cases with various complications including death. [7][8][9] We present a case of takotsubo cardiomyopathy in a female patient who suffered a fatal LV free wall rupture and the results of a comprehensive histopathologic investigation. Case ReportAn 81-year-old woman with hypertension started to feel chest pains after a quarrel with her son. Next day stomach pains and diarrhea appeared but the chest pain became intermittent, and the symptoms were accompanied by general fatigue. On the third day she was admitted to hospital because of chest discomfort at rest and ECG signs of ST-segment elevation myocardial infarction (MI) (Fig 1A). She had no history of prior angina or MI and no family history of heart disease and sudden death. On admission her heart rate was 104 beats/min, and blood pressure was 150/90 mmHg. Auscultation of the heart and lungs was normal, abdominal and neurological examination findings were negative, and there was no peripheral edema. Immediate coronary angiography did not reveal any significant coronary artery stenosis ( Figs 2A,B); the TIMI frame counts for the left anterior descending, circumflex and right coronary arteries were 29, 20 and 26 frames, respectively. However, ventriculography revealed a balloon-like LV motion abnormality with akinesis from the mid to apical portions and hyperkinesis of the base (Figs 2C,D). The LV end-systolic and end-diastolic pressureas were 150 mmHg and 15 mmHg, respectively, and there was no pressure gradient from the apex and midportion to the outflow tract; other hemodynamic data and the laboratory data on admission are shown in Table. After angiography the patient reported pain relief and was taken to the intensive care unit; however, the ECG recording showed no restoration of normal ST-segment (Fig 1B). The woman was stable during the first 40 h of admission, with no hemodynamic or arrhythmic problems, and she was given -blocker (metoprolol), angiotensin-converting enzyme inhibitor (ramipril) and aspirin; her blood pressure was within normal limits. She occasionally complained of chest discomfort; her creatine kinase-MB was maximal on admission and gradually diminished in further examinations, but the ST segment remained elevated ( Figs 1C,D). After 40 h of admission she reported a sudden pain in the epigastric region and the symptoms of acute abdomen soon appeared (C-reactive protein reached 267 mg/dl). After surgical consultation the woman was taken to the operation room for urgent surger...

“…20 In addition, a base-to apex perfusion gradient, similar to that described in patients with coronary risk factors, 21 could result in regional differences in myocardial blood flow in the setting of catecholamine-mediated microvascular dysfunction. This irregularity of the density of adrenoceptors in the LV combined with catecholamine-mediated microvascular dysfunction could create a wall motion similar to 'apical ballooning'.…”

Section: Discussionmentioning

confidence: 95%

Local Release of Catecholamines From the Hearts of Patients With Tako-Tsubo-Like Left Ventricular Dysfunction

Kume

Kawamoto

Okura

et al. 2008

160

ako-tsubo-like left ventricular (LV) dysfunction ischaracterized by a unique morphologic feature on the left ventriculography (LVG) and clinical features that include a predominance of elderly women, as well as a favorable prognosis. [1][2][3][4][5][6][7] The LV wall motion abnormality is localized to the LV apical region (LV apical ballooning), and improves within several weeks. Although tako-tsubolike LV dysfunction sometimes mimics myocardial infarction (MI) with respect to its symptoms and electrocardiographic (ECG) changes, it is quite different because there is a lack of organic epicardial coronary artery occlusion. Recent studies have shown that patients with this disease have evidence of exaggerated sympathetic activation, with plasma catecholamine levels several times higher than those in age-and sex-matched patients with Killip class III MI. 8 Therefore, catecholamines may play an important part in the occurrence of this entity. However, whether the catecholamines are released from cardiac sympathetic efferent neurons in patients with tako-tsubo-like LV dysfunction remains poorly understood, so the purpose of this study was to investigate evidence of local release of catecholamines from the heart in patients with tako-tsubo-like LV dysfunction. MethodsFive consecutive patients (3 females, 2 males) were examined. All had complained of chest pain/discomfort and were diagnosed with tako-tsubo-like LV dysfunction according to the following criteria: (1) LV wall motion abnormality at the apex on LVG; (2) ST-segment elevation or T-wave abnormality in at least 2 contiguous ECG leads; (3) no history of prior MI; (4) normal coronary angiogram (luminal narrowing <25% in all 3 coronary arteries). [1][2][3][4][5][6][7] The presence or absence of coronary risk factors, such as hypertension, hyperlipidemia, diabetes mellitus, and smoking were determined. The study protocol was approved by the Ethics Committee of Kawasaki Medical School, and written informed consent was given by each patient. LVG and coronary angiography (CAG) were performed by the femoral approach after intravenous infusion of 5,000 U heparin. The LV end-diastolic pressure was obtained following LVG. The LV ejection fraction was calculated by the area -length method. 9 After confirming the LV apical wall motion abnormality and normal CAG, sampling of blood for the measurement of plasma catecholamine levels was performed from the aortic root (Ao) and coronary sinus (CS). Plasma catecholamine levels were determined through high-performance liquid chromatography. Serum creatine kinase (CK) level was measured every 3 h after admission and the peak value was recorded. Patients received standard drug therapy (eg, diuretics or vasodilator therapy) according to the attending cardiologist's discretion. After 3 weeks, follow-up LVG were performed in the same way as before. ResultsThe median age of the patients was 76 years (range 71-78) and 60% were women (Table 1). The patients reported a variety of causes of emotional or physical stress (case 1: operation o...