Sympathetic activity and myocardial damage after stimulation of dorsal medulla and vagotomy in a novel animal model

Chiu, Yung-Tsung; Chen, Ying‐Tsung; Lin, Nai-Nu; Cheng, Ching-Chang; Gong, Chi Li; Cheng, Fu‐Chou; Hsu, Shih-Lan; Chi, Ching‐Shiang; Fu, Yun‐Ching

doi:10.1016/j.ijcard.2004.08.026

Cited by 12 publications

(8 citation statements)

References 30 publications

(83 reference statements)

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“…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. 17 That animal model of sympathetic hyperexcitation corresponds very well to both the functional and pathological features of takotsubo cardiomyopathy in humans. Nevertheless, we did not measure the patient's cathecholamine level, so it is hard to conclude that sympathetic hyperactivity and catecholamine excess caused the cardiac damage in the present case.…”

Section: Discussionmentioning

confidence: 93%

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

Sacha¹,

Maselko²,

Wester³

et al. 2007

Circ J

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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...

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Section: Discussionmentioning

confidence: 93%

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

Sacha¹,

Maselko²,

Wester³

et al. 2007

Circ J

View full text Add to dashboard Cite

show abstract

“…Therefore, adrenaline production is decreased without glucocorticoids, as in our case. We consider that increased noradrenaline levels or activation of the sympathetic nervous system contributed to the damage of cardiac myocytes causing cardiomyopathy in our case, because stimulation of the sympathetic nervous system would induce apoptosis or damage to the cardiac myocytes [16,17].…”

Section: Discussionmentioning

confidence: 96%

Ampulla (Takotsubo) Cardiomyopathy Caused by Secondary Adrenal Insufficiency in ACTH Isolated Deficiency

et al. 2007

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Abstract. We describe here a case of reversible ampulla (takotsubo) cardiomyopathy caused by secondary adrenal insufficiency in ACTH isolated deficiency. A 53-year-old woman was referred to our department for evaluation and treatment of unconsciousness. On admission, her plasma glucose level was 34 mg/dL, suggesting loss of consciousness due to hypoglycemia. Basal levels of ACTH, cortisol, and dehydroepiandrosterone sulfate in blood, and urinary free cortisol levels were all decreased. ACTH and cortisol levels were not adequately increased in response to CRH administration and the insulin tolerance test. Electrocardiography showed ST segment elevation and T wave inversion in leads V 1-6 . The coronary arteries were free of organic stenosis, and a left ventriculogram revealed severe hypokinesis, particularly in the anterior and posterior walls. Based on a diagnosis of adrenocortical insufficiency caused by ACTH isolated deficiency, hydrocortisone was administered. Two weeks after treatment, ultrasound studies of the heart showed recovery of left ventricular wall motion. Activation of the sympathetic nervous system, adrenocortical failure, and hypoglycemic attack were considered to be triggering factors for the takotsubo cardiomyopathy. Careful monitoring of cardiac function and appropriate treatments for both cardiomyopathy and adrenocortical failure are required to recover cardiac dysfunction.

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“…Therefore, other mechanisms should be considered to explain the relationship between myocardial damage and AF. Cardiac sympathetic nervous activation is associated with myocardial injury (17). Furthermore, AF-induced sympathetic nervous disintegrity is one process underlying the progression of myocardial damage.…”

Section: Mechanisms Of Myocardial Damage In Af Patientsmentioning

confidence: 99%

Prognostic Value of Myocardial Damage Markers in Patients with Chronic Heart Failure with Atrial Fibrillation

et al. 2014

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Objective The aim of the present study was to examine the relationship between myocardial damage caused by atrial fibrillation (AF) and subsequent cardiovascular events in AF patients with chronic heart failure (CHF). Methods and ResultsWe measured the serum levels of heart-type fatty acid binding protein (H-FABP) and high-sensitivity troponin T in 402 consecutive CHF patients with chronic AF (CHF-AF, n=201) or sinus rhythm (CHF-SR, n=201). The patients with CHF-AF had higher H-FABP and troponin T levels than those with CHF-SR. In order to examine the prognostic value of myocardial damage markers in CHF-AF and CHF-SR patients, we followed the above patients and analyzed their clinical outcomes. A multivariate Cox proportional hazard analysis revealed that both the serum H-FABP and troponin T levels independently predicted subsequent cardiovascular events. A Kaplan-Meier analysis demonstrated that the rate of cardiovascular events was higher in the patients with elevated H-FABP and troponin T levels. The optimal cut-off values for the myocardial damage markers of cardiovascular events were higher in the CHF-AF patients than in the CHF-SR patients (H-FABP, 5.4 vs. 4.6 ng/mL and troponin T, 0.030 vs. 0.013 ng/mL). Conclusion Myocardial damage advances in association with the presence of AF and is associated with subsequent cardiovascular events in both CHF-AF and CHF-SR patients. In this study, the cut-off values for the myocardial damage markers were higher in the CHF-AF patients than in the CHF-SR patients.

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Sympathetic activity and myocardial damage after stimulation of dorsal medulla and vagotomy in a novel animal model

Cited by 12 publications

References 30 publications

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

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

Ampulla (Takotsubo) Cardiomyopathy Caused by Secondary Adrenal Insufficiency in ACTH Isolated Deficiency

Prognostic Value of Myocardial Damage Markers in Patients with Chronic Heart Failure with Atrial Fibrillation

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