Hypertension in patients with pheochromocytoma

Adrenal-dependent hypertension syndromes are uncommon forms of hypertension. They include primary aldosteronism, pheochromocytoma, Cushing’s syndrome, and congenital adrenal hyperplasia. Pheochromocytomas are the cause of hypertension in 0.1% to 0.2% of hypertensive patients. Excess catecholamine release and other neural and humoral mechanisms contribute to the pathophysiology of hypertension. Patients with pheochromocytomas have a potentially curable cause of endocrine hypertension and, if undetected, pheochromocytomas confer a high risk for morbidity and mortality, especially during surgical procedures and pregnancy. All patients with incidental adrenal tumors, regardless of tumor size, should be biochemically screened for pheochromocytoma (especially before resection or needle biopsy) to avoid precipitation of a lethal hypertensive crisis.     

Carotid vascular remodeling in patients with pheochromocytoma

CONTEXT: The influence of catecholamines on vascular remodeling in humans was investigated. OBJECTIVE: The objective was to study the carotid vascular wall in patients with pheochromocytoma (PHEO). DESIGN AND SETTING: An observational study was conducted in a university referral center for blood pressure diseases. PATIENTS: Fourteen patients with PHEO, 15 matched high-normal essential hypertensives, 15 mild essential hypertensives, and 15 controls underwent two-dimensional conventional ultrasonography and ultrasonic tissue characterization of the carotid wall. MAIN OUTCOME MEASURES: Intimal media thickness (IMT), diameter, and corrected ultrasonic integrated backscatter signal (C-IBS) of carotid arteries were evaluated. RESULTS: IMT in PHEOs (0.844 +/- 0.18 mm, mean +/- sd) was greater than not only controls (0.596 +/- 0.09 mm, P < 0.0002) but also high-normal (0.710 +/- 0.17 mm, P < 0.03), and even mild (0.727 +/- 0.20 mm, P = 0.06) hypertensives. IMT in the latter was higher than in controls (P < 0.03), without difference in comparison with high-normal hypertensives. C-IBS values in PHEOs (-21.71 +/- 2.0 dB, mean +/- sd) were greater than in controls (-26.20 +/- 1.73 dB, P < 0.0001) but also than in high-normal (-23.84 +/- 1.16 dB, P < 0.002) and mild (-23.37 +/- 1.99 dB, P < 0.01) hypertensives. C-IBS values in controls were lower than in high-normal (P < 0.0005) and mild (P < 0.0001) hypertensives. Carotid diameter was not significantly different in the four groups. In PHEOs, C-IBS was associated with urinary noradrenaline (r = 0.640, P < 0.01) and normethanephrine (r = 0.737, P < 0.009). CONCLUSIONS: Carotid IMT of PHEOs is higher than in controls and matched groups of hypertensives with comparable or even higher blood pressure. This vascular rearrangement is characterized by increased IBS values due to collagen deposition and vascular fibrosis. Therefore, our data show that abnormal catecholamine levels take part per se in carotid wall remodeling of patients with PHEO.     

Postural ventricular tachycardia in patients with pheochromocytoma

Many kinds of cardiac complications have been reported in association with pheochromocytoma, including transient ECG changes, catecholamine-induced myocardial injury and various types of supraventricular or ventricular tachyarrhythmias. We report a case admitted to our hospital for evaluation of ventricular tachycardia. A 45-year old woman entered the cardiology department with the complaint of recurrent palpitation in a position of ante-flexion. Physical examination at a time of admission revealed a regular pulse of 62/min, blood pressure of 100/56 mmHg (sitting). There was no evidence of cardiac enlargement or congestive heart failure. An ambulatory 24 hour ECG showed recurrent ventricular tachycardia short run with wide QRS at the time of ante-flexion. Urea, electrolytes and complete blood count were normal. Serum cardiac enzymes, thyroid function tests and glucose were normal. An echocardiogram confirmed no specific changes, such as left ventricular hypertrophy. 24 hour urine collection confirmed an elevated vanillylmandelic acid (10.4 micrograms/day: normal 2.0-2.8), metanephrine (0.68 micrograms/day: normal 0.04-0.18) and normetanephrine (1.71 micrograms/day: normal 0.1-0.28). Serum catecholamine level showed adrenalin, 0.26 ng/ml: normal less than 0.12) and noradrenaline (3.34 ng/ml: normal 0.1-0.41). These values increased to 1.34 and 24.75 respectively during palpitation attack. Abdominal enhanced computed tomography showed a 3 cm diameter tissue mass in the left adrenal area. Surgical resection of this pheochromocytoma was accomplished uneventfully. It was successfully excised and the patient was discharged in good health two weeks after the operation. Cardiotoxic effects of catecholamines have been well described by many investigators. In our case, tachyarrhythmia was induced without excessive changes of ECG findings. In patients with pheochromocytoma, occurrence of various types of cardiac arrhythmia should be considered.     

Reversible cerebral ischemia in patients with pheochromocytoma

Cerebral ischemia and symptoms of stroke can occur as a rare manifestation in patients with pheochromocytoma. We describe a 45-year-old woman who was admitted because of a right-sided hemiparesis due to an ischemic lesion in the left hypothalamus. The clinical diagnosis of a pheochromocytoma was proven by highly elevated urinary catecholamines and confirmed histologically after operation. The successful removal of the tumor led to the almost complete recovery of the neurological deficiencies. It is of vital importance to know this atypical presentation of pheochromocytoma. The diagnosis of pheochromocytoma should be suspected in patients with focal cerebral symptoms, particularly in the presence of intermittent hypertension or other paroxysmal symptoms suggestive of pheochromocytoma.     

Direct blood pressure monitoring in patients with pheochromocytoma

In patients with pheochromocytoma, blood pressure was monitored continuously for 2 days using direct measurement techniques. Systolic blood pressure sometimes increased to more than 300 mmHg. These sudden elevations of blood pressure were associated with increased levels of plasma catecholamines. Pre-operative prazosin and propranolol therapy lowered mean systolic and diastolic blood pressure throughout the 2 day observation periods and was associated with decreased hematocrit levels. However, these agents did not prevent the rapid elevation of blood pressure.     

Source of plasma adrenomedullin in patients with pheochromocytoma

Controversy exists as to the origin of plasma adrenomedullin (AM). To elucidate the source of plasma AM, we measured two molecular forms of AM, an active form of mature AM (AM-m) and an intermediate inactive form of glycine-extended AM (AM-Gly), by immunoradiometric assay using specific kits in two female patients with pheochromocytoma before and 3 weeks after surgery. We also measured plasma AM-m, AM-Gly, and AM-T (AM-m + AM-Gly) levels, in addition to plasma epinephrine (E) and norepinephrine (NE) levels, in bilateral adrenal veins of one patient. Although plasma E and NE levels decreased markedly after surgery in these patients, changes in plasma AM appeared to be confined to the normal range. There were no obvious differences in plasma AM-T, AM-m, or AM-Gly levels in adrenal veins between healthy tissue and tumor sides. Furthermore, plasma AM-T, AM-m, or AM-Gly levels in adrenal veins were comparable with those in the infrarenal inferior vena cavae (IVC) or the suprarenal IVC. In contrast, plasma E and NE levels increased in the adrenal vein of the healthy side and increased further in the adrenal vein of the tumor side compared with those in the infrarenal IVC. These results suggest that the origin of plasma E and NE is the adrenal gland and that elevated plasma levels of E and NE in pheochromocytoma are due to excessive production of E and NE in the adrenal gland of the tumor side. In contrast, it is suggested that neither plasma AM levels in the adrenal vein of the healthy side nor those of the tumor side contribute to the systemic levels of plasma AM. The present results appear to be consistent with the hypothesis that the source of circulating AM is systemic vasculature.     

嗜铬细胞瘤患者血浆醛固酮浓度的变化

目的:探讨嗜铬细胞瘤患者血浆醛固酮浓度的变化特点。方法:回顾性分析我院近5年经手术病理证实或临床确诊的21例嗜铬细胞瘤患者的临床资料,并选择年龄、性别相匹配的同期住院确诊的原发性高血压患者21例,通过配对比较,研究嗜铬细胞瘤患者血浆立位、卧位醛固酮浓度的变化特点。结果:(1)嗜铬细胞瘤患者与原发性高血压患者入院时的收缩压及舒张压水平均无明显差别(P>0.05);(2)嗜铬细胞瘤患者血浆立位、卧位醛固酮浓度均高于原发性高血压患者(P<0.05)。结论:嗜铬细胞瘤患者血浆立位、卧位醛固酮浓度升高,对嗜铬细胞瘤的定性诊断具有一定的价值。     

嗜铬细胞瘤20例临床分析

目的：探讨嗜铬细胞瘤临床特点，提高诊治水平。方法：对20例嗜铬细胞瘤的临床资料总结分析。结果：20例均经手术治疗，单侧17例，家族性双侧3例，恶性嗜铬细胞瘤4例，肾上腺外嗜铬细胞瘤1例，无症状嗜铬细胞瘤4例。结论：嗜铬细胞瘤典型表现是高血压、头痛、心悸和出汗，而无症状性、家族性和其他非典型的特殊表现需引起注意。儿茶酚胺及影像学检查是主要的诊断手段。     

Characteristics of systolic time intervals in patients with pheochromocytoma

The effect of chronic catecholamine excess on cardiac function was assessed in 8 patients with surgically proven pheochromocytoma and the results compared with data obtained from normal controls and essential hypertensives. Major findings in systolic time intervals (STI) in patients with pheochromocytoma were a marked shortening of electromechanical systole and left ventricular ejection time (ET), but pre-ejection period (PEP) remained within normal limits. These findings were not altered by correction for heart rate. The ET/PEP ratio was very low (1.87 +/- 0.31) due to the remarkable shortening of ET. The ET/PEP ratio in essential hypertensives was also low (1.77 +/- 0.38), but this was mainly due to a remarkable prolongation of PEP. Low cardiac index, low stroke index and high total peripheral resistance index were preoperative characteristics in patients with pheochromocytoma, but returned to normal after operation. These results suggest that chronic excessive production of catecholamines from pheochromocytoma has deleterious effects on the heart, and that wide differences in STI exist between patients with pheochromocytoma and those with essential hypertension.     

Hypertension in patients presenting with stroke

Hypertension is a major risk factor for stroke disease. There is now some international agreement on what constitutes hypertension, and at what level of blood pressure treatment is required. Large randomised controlled trials demonstrate the benefit of reducing blood pressure for the primary and secondary prevention of stroke disease. Studies have also demonstrated the benefit of particular classes of antihypertensive agents in certain patient groups. Research is beginning to elucidate the problems of hypertension in the acute phase of ischaemic stroke and the therapeutic strategies that may be helpful. Given the significant impact of stroke disease on all health services, it remains an important priority to determine the best management of hypertension in stroke.     

Hypertension in patients presenting with epistaxis

STUDY OBJECTIVE: We sought to evaluate whether patients with epistaxis in the emergency department have a higher arterial blood pressure compared with patients with other medical emergencies and to study the association of elevated blood pressure during epistaxis with sustained arterial hypertension. METHODS: In a prospective, cross-sectional, prevalence study we compared arterial blood pressure on admission in the ED in 213 consecutive patients treated for epistaxis with that of 213 sex- and age-matched control subjects. In 33 of those patients with elevated blood pressure during epistaxis, we evaluated the prevalence of sustained arterial hypertension. Main outcome measures were arterial blood pressure during epistaxis and evidence of sustained arterial hypertension, as determined by 24-hour ambulatory blood pressure measurement. RESULTS: Patients with epistaxis had significantly higher blood pressure values compared with those of control patients (systolic blood pressure 161+/-30 versus 144+/-22 mm Hg, P<.001; diastolic blood pressure 84+/-19 versus 75+/-15 mm Hg, P <.001). Of 33 (30%) of 108 patients with elevated blood pressure during epistaxis who were further evaluated, 26 (79%) patients were classified as having sustained arterial hypertension. Nine (27%) patients with sustained arterial hypertension were unaware of a history of hypertension. Patients with sustained arterial hypertension had significantly more episodes of epistaxis compared with patients with elevated blood pressure during epistaxis and no sustained arterial hypertension (mean 5 versus 1; P=.004). CONCLUSION: Patients with epistaxis have a higher blood pressure compared with that of control patients. Twenty-six (79%) of 33 patients with elevated blood pressure during epistaxis had sustained arterial hypertension. Nine (27%) of these patients were unaware of a history of hypertension. Continued management of patients with epistaxis and high blood pressure should include confirmation or exclusion of sustained arterial hypertension by 24-hour ambulatory blood pressure recording.     

Hypertension in patients presenting with stroke

Hypertension is a major risk factor for stroke disease. There is now some international agreement on what constitutes hypertension, and at what level of blood pressure treatment is required. Large randomised controlled trials demonstrate the benefit of reducing blood pressure for the primary and secondary prevention of stroke disease. Studies have also demonstrated the benefit of particular classes of antihypertensive agents in certain patient groups. Research is beginning to elucidate the problems of hypertension in the acute phase of ischaemic stroke and the therapeutic strategies that may be helpful. Given the significant impact of stroke disease on all health services, it remains an important priority to determine the best management of hypertension in stroke.