Cardiovascular complications in patients with pheochromocytoma: A mini-review

Galetta, Fabio; Franzoni, Ferdinando; Bernini, Giampaolo; Poupak, Fallawi; Carpi, Angelo; Cini, G; Tocchini, Leonardo; Antonelli, Alessandro; Santoro, Gino

doi:10.1016/j.biopha.2009.09.014

Cited by 103 publications

(67 citation statements)

References 63 publications

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“…They include LV hypertrophy, myocardial infarction, arrhythmias, heart failure, and cardiogenic shock. 1 In this case, a patient with an undiagnosed pheochromocytoma developed a symptomatic dilated cardiomyopathy and severe left-sided heart failure after initiation of ␤ blockade with propranolol. The subsequent rapid structural and functional recovery of the myocardium after appropriate ␣ blockade was administered highlights the importance of ␣ blockade and its dramatic effect toward improving LV function in this setting.…”

Section: Discussionmentioning

confidence: 88%

Severe Dilated Cardiomyopathy After Propranolol Treatment in an Undiagnosed Adrenal Pheochromocytoma

McEntee

Coyle

Meyer

2011

Circ: Heart Failure

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A 43-year-old woman presented to an outside hospital with 3 hours of newly onset substernal chest pressure, associated nausea, vomiting, shortness of breath, palpitations, and diaphoresis. Her medical history was significant for 18 months of episodic headaches that were diagnosed as atypical migraines and being treated with daily propranolol 60 mg initiated 1 week before the current presentation. Blood pressure on presentation was 144/112 mm Hg, initial ECG showed T-wave inversions in leads I and aVL ( Figure 1A), and troponin I level was 0.497 ng/mL (normal, Ͻ0.034 ng/mL). The chest pain was relieved by nitroglycerin infusion, which was discontinued after 40 minutes secondary to a decrease in blood pressure to 95/72 mm Hg. The patient was treated with aspirin, clopidogrel, and heparin and transferred to our hospital for urgent left heart catheterization.On presentation to our hospital, blood pressure was 97/ 50 mm Hg, troponin I was 4.54 ng/mL (positive, Ͼ0.8 ng/mL), and the ECG showed partial resolution of T-wave inversion and sinus tachycardia ( Figure 1B). Coronary angiography showed no clinically significant coronary artery disease. Transthoracic echocardiogram revealed moderate dilation of the left ventricle (LV), diffuse LV hypokinesis, and moderate to severely decreased LV function with an LV ejection fraction of 25% to 30%. The patient developed symptomatic hypotension to 75/55 mm Hg with tachycardia and was transferred to the intensive care unit. A central venous catheter was placed, and she was monitored closely for further hemodynamic instability. She stabilized without further intervention. Plasma fractionated metanephrines were drawn on hospital day 3 to evaluate for pheochromocytoma given the patient's history of episodic tachycardia, headache, and diaphoresis. Carvedilol 3.125 mg and lisinopril 5 mg were started. She remained hemodynamically stable and asymptomatic and was discharged home on hospital day 4 with carvedilol 3.125 mg BID and lisinopril 10 mg daily with plans to follow up with outpatient cardiology.On the day of discharge, the patient was symptomatic at home with palpitations, diaphoresis, presyncope, and a selfmeasured blood pressure of 160/110 mm Hg. A 24-hour Holter monitor was placed, which was negative, although she was asymptomatic during the monitoring period. On postdischarge day 3, laboratory results returned abnormal plasma fractionated metanephrines; these results were followed up with a 24-hour urine test, which also was markedly elevated (Table). Abdominal CT showed a 3.5ϫ2.9ϫ2.7-cm right-side adrenal mass (Figure 2A). Medical treatment was changed to metoprolol succinate 25 mg daily, phenoxybenzamine 10 mg daily, and lisinopril 15 mg daily. Repeat transthoracic echocardiogram 1 month after presentation and 2 weeks after initiating phenoxybenzamine therapy showed normal LV systolic function with an LV ejection fraction of 65% to 70% without wall motion abnormalities. Two months after initial presentation, the patient underwent laparoscopic adrenalectomy after preoperati...

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Section: Discussionmentioning

confidence: 88%

Severe Dilated Cardiomyopathy After Propranolol Treatment in an Undiagnosed Adrenal Pheochromocytoma

McEntee

Coyle

Meyer

2011

Circ: Heart Failure

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“…Estos mecanismos son responsables del atontamiento miocárdico y las anormalidades en la motilidad segmentaria 8 .…”

Section: Discussionunclassified

Feocromocitoma: presentación como síndrome coronario agudo. Reporte de un caso

Enríquez¹,

Paredes

Tagle

et al. 2014

Rev. méd. Chile

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Refería haber presentado episodio de similares características dos días antes, lo que motivó consulta en otro servicio de urgencias, donde fue evaluada con electrocardiograma (ECG) y enzimas cardiacas; no impresionando cuadro de origen coronario, por lo que se derivó a su domicilio. Dentro de sus antecedentes destacaba historia de hipertensión arterial de data no precisada, en tratamiento con atenolol 50 mg al día, y cáncer de mama tratado 20 años antes con cirugía y radioterapia. La paciente no era fumadora ni tenía antecedentes familiares de cardiopatía coronaria.Al ingreso, la paciente se encontraba sudorosa, pero sin dolor. La presión arterial era 100/60 mmHg y su frecuencia cardiaca 87 lpm. Al examen físico destacaban yugulares colapsables en inspiración, la auscultación cardiaca no reveló soplos ni galope y había sensibilidad a la palpación epigástrica. El resto del examen no era destacable. Al interrogatorio, la paciente refería historia de episodios similares durante los últimos 6 meses, sin clara relación con esfuerzos físicos, que en un principio eran esporádicos pero que durante la última semana se hicieron más frecuentes, casi diarios. El ECG mostró un discreto supradesnivel del segmento ST (SDST) anteroseptal con inversión de la onda T de V1 a V3, que ya era evidente en ECG tomado 2 días antes y que no fue evolutivo (Figura 1). La radiografía de tórax mostró una silueta cardiaca de tamaño normal y no se observaban signos de congestión pulmonar. La paciente fue admitida a la unidad coronaria, con terapia de síndrome coronario agudo sin SDST. La troponina I de ingreso fue de 0,07 pg/ml (valor normal < 0,05) y la CK

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“…Typically it expresses itself as a triad of abrupt episodes of headache, palpitations, and profuse sweating, accompanied by either sustained or paroxysmal hypertension or a labile blood pressure [1]. However, several case reports illustrate unexpected onset of the disease with failure of organs and systems, including multiple organ failure, as well as severe cardiovascular disorders, including life-threatening arrhythmias [2][3][4][5][6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%