Free noradrenaline and adrenaline excretion in relation to clinical syndromes following myocardial infarction

Valori, C; Thomas, Michael; Shillingford, John

doi:10.1016/0002-9149(67)90001-x

Cited by 202 publications

(44 citation statements)

References 13 publications

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“…One patient in this group had crises related to a cerebrovascular accident, known to be imitative of pheochromocytoma; 23 another had crises probably related to an atypical coronary insufficiency, an association also previously described. 24 Four of the five Group 2 patients suspected of having a pheochromocytoma had conjugated NE + E far below the mean of the whole group; they may thus represent borderline cases between Groups 1 and 2.…”

Section: -Umentioning

confidence: 94%

Essential hypertension with low conjugated catecholamines imitates pheochromocytoma.

Kuchel¹,

Buu²,

Hamet³

et al. 1981

Hypertension

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SUMMARYThe correlation between the degree of conjugation of plasma noreplnephrine (NE) and epinepbrine (E) and the clinical features of sympathetic hyperactivity was studied in 38 essential hypertensive patients from a referral population biased toward pheochromocytoma (19 of them suspected of this diagnosis on clinical grounds). The patients were separated into two groups: 15 with subnormal plasma conjugated NE + E, i.e., below 0.23 ng/ml (Group 1), and 23 patients above this limit (Group 2). Patients clinically suspected of pheochromocytoma represented 93% of the patients in Group 1 but only 21% in Group 2.Group 1 patients, compared to those of Group 2, had: 1) higher baseline plasma free NE + E (0.51 ± 0.07 ng/ml vs 0.30 ± 0.04 ng/ml,p < 0.02); 2) an increase in plasma free NE + E in response to stressful sampling (148% ± 59%, p < 0.05 vs 58% ± 30%), and a more pronounced response (p < 0.05) to glucagon administration; 3) higher free NE + E and DA in the regional samples received during catheterization while conjugated NE and/or E were usually absent; and 4) a higher spread between maximum and minimum blood pressure and a higher maximum pulse rate recorded as well as the index of sympathotonia. All patients combined had the 'maximum pulse rate correlated negatively (p < 0.005) with conjugated NE + E, but positively (p < 0.005) with free NE + E. The clinical and biochemical similarity to pheochromocytoma was particularly striking in some Group 1 patients who had a selective defect in E conjugation; some of them had a history of surgical exploration for the lesion, without result.The association of subnormal conjugated plasma NE and/or E with moderately elevated plasma NE + E and a more frequent pseudopheochromocytoma presentation may result from inadequate conjugation, and hence inactivation of NE and/or E. Excessive free catecholamines would account for the clinical symptoms and for tbe fact that the patients are well controlled by treatment with beta-adrenerglc blocking agents, either alone or in combination with a-blockers. Awareness of tbe existence of this variety of essential hypertension can obviate unnecessary surgery for wrongly suspected pheochromocytoma. (Hypertension 3: 347-355, 1981) KEY WORDS • hypertension • catecholamine conjugation defect • pseudopheochromocytomaA N important mechanism for the inactivation of catecholamines (CA) is conjugation, yet this mechanism is poorly explored. In man, conjugation is mainly to sulfates. Circulating norepinephrine (NE) and epinephrine (E) are 80% conjugated (although it is usually the free form that is determined); circulating dopamine (DA) is almost entirely in the conjugated form.

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Section: -Umentioning

confidence: 94%

Essential hypertension with low conjugated catecholamines imitates pheochromocytoma.

Kuchel¹,

Buu²,

Hamet³

et al. 1981

Hypertension

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“…Major metabolic changes occur during the early hours of AMI 20 ; these include increased secretion of catecholamines, 21 increased concentration of circulating free fatty acids (FFA), 22 and glucose intolerance. 23 Each of these abnormalities might adversely influence the outcome of AMI, either by provoking arrhythmias or by compromising the survival of ischemic tissue.…”

Section: Proposed Mechanism Of Action Of Gikmentioning

confidence: 99%

“…24,25 Under normal conditions, myocardium depends on aerobic metabolism, and the preferred fuels for myocardial oxidative metabolism are FFA. 26 The high concentration of FFA during the early stages of AMI, a consequence of high sympathetic activity, 21 could be deleterious, increasing the incidence of potentially malignant arrhythmias 22 and adversely influencing the outcome of ischemic but viable tissue. 24,25 A detailed review of the mechanism of action of GIK has recently been written by Apstein and Taegtmeyer.…”

Section: Proposed Mechanism Of Action Of Gikmentioning

confidence: 99%

Metabolic Modulation of Acute Myocardial Infarction

Dı́az

Ea²,

Ls³

et al. 1998

Circulation

406

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on behalf of the ECLA (Estudios Cardiológicos Latinoamérica) Collaborative Group* Background-Several trials have been performed in the past using glucose, insulin, and potassium infusion (GIK) for the treatment of acute myocardial infarction (AMI). Because of continuing uncertainty about the potential role of this therapeutic intervention, we conducted a randomized trial to evaluate the impact of a GIK solution during the first hours of AMI. Methods and Results-Four hundred seven patients with suspected AMI admitted within 24 hours of symptoms onset were enrolled. In a ratio of 2:1, 268 patients were allocated to receive GIK (high-or low-dose) and 139 to receive control. Phlebitis and serum changes in the plasma concentration of glucose or potassium were observed more often with GIK. A trend toward a nonsignificant reduction in major and minor in-hospital events was observed in patients allocated to GIK. In 252 patients (61.9%) treated with reperfusion strategies, a statistically significant reduction in mortality (relative risk [RR] 0.34; 95% CI: 0.15 to 0.78; 2Pϭ0.008) and a consistent trend toward fewer in-hospital events in the GIK group were observed. Conclusions-Our results confirm that a metabolic modulation strategy in the first hours of an AMI is feasible, applicable worldwide, and has mild side effects. The statistically significant mortality reduction in patients who underwent a reperfusion strategy might have important implications for the management of AMI patients. It is now essential to perform a large-scale trial to reliably determine the magnitude of benefit.

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“…[9][10][11][12][13][14] Patients with acute myocardial infarction frequently exhibit excessive adrenergic activity as evidenced by an elevation of plasma and 24-hour urinary catecholamines. [15][16][17][18][19][20][21][22][23] It was therefore hypothesized that the abbreviated electromechanical systole characteristic of patients with myocardial infarction is a direct reflection of increased sympathetic nervous system activity. The.present investigation was designed to test this hypothesis.…”

Section: Ine Excretionmentioning

confidence: 99%

Shortening of Electromechanical Systole as a Manifestation of Excessive Adrenergic Stimulation in Acute Myocardial Infarction

et al. 1972

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Free noradrenaline and adrenaline excretion in relation to clinical syndromes following myocardial infarction

Cited by 202 publications

References 13 publications

Essential hypertension with low conjugated catecholamines imitates pheochromocytoma.

Essential hypertension with low conjugated catecholamines imitates pheochromocytoma.

Metabolic Modulation of Acute Myocardial Infarction

Shortening of Electromechanical Systole as a Manifestation of Excessive Adrenergic Stimulation in Acute Myocardial Infarction

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