Plasma levels of atrial natriuretic peptide during myocardial ischemia induced by percutaneous transluminal coronary angioplasty or dynamic exercise

Ikäheimo, Markku J.; Ruskoaho, Heikki; Airaksinen, Juhani; Huikuri, Heikki V.; Korhonen, Ulla R.; Leppäluoto, P.J.; Tuominen, M.; Takkunen, Juha T.

doi:10.1016/0002-8703(89)90620-0

Cited by 28 publications

(6 citation statements)

References 24 publications

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“…Plasma atrial natriuretic peptide (ANP), the amino‐terminal fragment of the pro‐atrial natriuretic peptide precursor (NT‐proANP), and BNP levels may be elevated on admission with acute myocardial infarction (AMI) 9–11 . Plasma ANP level may also show a transient rise during myocardial ischaemia associated with coronary angioplasty 12–14 . Kikuta et al have reported elevated plasma BNP levels, but not ANP levels, in patients with unstable angina associated with ECG evidence of ischaemia 15 …”

Section: Introductionmentioning

confidence: 99%

Plasma amino‐terminal pro‐brain natriuretic peptide levels in subjects presenting to the Emergency Department with suspected acute coronary syndrome: possible role in selecting patients for follow up?

Campbell

Munir²,

Hennessy

et al. 2001

Internal Medicine Journal

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Although elevated NT-proBNP level detected heart failure with high sensitivity, NT-proBNP level did not assist in the diagnosis of acute myocardial ischaemia. These findings indicate that the major determinant of elevated NT-proBNP level on presentation with suspected ACS was underlying cardiac dysfunction rather than acute myocardial ischaemia. This suggests that NT-proBNP measurement in patients with a suspected cardiac reason for presentation to the Emergency Department may identify a previously unrecognized group of patients without acute ischaemia who may nevertheless benefit from further investigation of cardiac function.

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Section: Introductionmentioning

confidence: 99%

Plasma amino‐terminal pro‐brain natriuretic peptide levels in subjects presenting to the Emergency Department with suspected acute coronary syndrome: possible role in selecting patients for follow up?

Campbell

Munir²,

Hennessy

et al. 2001

Internal Medicine Journal

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“…Tachycardia is also a stimulation to induce myocardial ischemia. It has been reported that myocardial ischemia per se enhances secretion of ANP in clinical as well as experimental studies (11,13,20,33). Myocardial ischemia has been repeatedly related to a pathophysiological background of HCM (3,6,27,30,34).…”

Section: Discussionmentioning

confidence: 99%

“…More importantly, the secretion of ANP was enhanced only in HCM patients with significant myocardial ischemia, suggesting a key role of myocardial ischemia in augmentation of ANP secretion in HCM. In patients with angina pectoris, ANP secretion has been reported to be increased with induction of myocardial ischemia by exercise (20), dipyridamole (13), and percutaneous transluminal coronary angioplasty (11). One plausible mechanism is that the elevated left atrial pressure caused by myocardial ischemia stimulates secretion of ANP.…”

Section: Discussionmentioning

confidence: 99%

Tachycardia-induced myocardial ischemia and diastolic dysfunction potentiate secretion of ANP, not BNP, in hypertrophic cardiomyopathy

Kido

Hasebe

Ishii

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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Kido, Shinsuke, Naoyuki Hasebe, Yoshinao Ishii, and Kenjiro Kikuchi. Tachycardia-induced myocardial ischemia and diastolic dysfunction potentiate secretion of ANP, not BNP, in hypertrophic cardiomyopathy. Am J Physiol Heart Circ Physiol 290: H1064 -H1070, 2006. First published September 19, 2005 doi:10.1152/ajpheart.00110.2005.-The aim of this study was to investigate what factor determines tachycardia-induced secretion of atrial and brain natriuretic peptides (ANP and BNP, respectively) in patients with hypertrophic cardiomyopathy (HCM). HCM patients with normal left ventricular (LV) systolic function and intact coronary artery (n ϭ 22) underwent rapid atrial pacing test. The cardiac secretion of ANP and BNP and the lactate extraction ratio (LER) were evaluated by using blood samples from the coronary sinus and aorta. LV end-diastolic pressure (LVEDP) and the time constant of LV relaxation of tau were measured by a catheter-tip transducer. These parameters were compared with normal controls (n ϭ 8). HCM patients were divided into obstructive (HOCM) and nonobstructive (HNCM) groups. The cardiac secretion of ANP was significantly increased by rapid pacing in HOCM from 384 Ϯ 101 to 1,268 Ϯ 334 pg/ml (P Ͻ 0.05); however, it was not significant in control and HNCM groups. In contrast, the cardiac secretion of BNP was fairly constant and rather significantly decreased in HCM (P Ͻ 0.01). The cardiac ANP secretion was significantly correlated with changes in LER (r ϭ Ϫ0.57, P Ͻ 0.01) and tau (r ϭ 0.73, P Ͻ 0.001) in HCM patients. Tachycardia potentiates the cardiac secretion of ANP, not BNP, in patients with HCM, particularly when it induces myocardial ischemia and LV diastolic dysfunction. left ventricular outflow tract obstruction; lactate extraction ratio; left ventricular diastolic function; cardiac event; atrial and brain natriuretic peptides THE CLINICAL SIGNIFICANCE of natriuretic peptides has been widely accepted in the management of heart failure. The plasma levels of brain natriuretic peptide (BNP) correlate well with the clinical severity of heart failure and hypertrophy (2,8,14). BNP is secreted mainly from the ventricle, whereas atrial natriuretic peptide (ANP) is produced and secreted not only from the atrium but from the ventricle in the hypertrophied heart (4, 23, 32). ANP synthesis is also enhanced in patients with heart failure (21, 36); however, the plasma ANP levels fluctuate more easily compared with BNP levels.The plasma levels of natriuretic peptides have been reported to be increased despite the intact contractile function of the left ventricle (LV) in patients with hypertrophic cardiomyopathy (HCM). The hypertrophied heart is prone to complicate with diastolic dysfunction (35). Tachycardia induces heart failure in patients with hypertrophied LV because diastolic dysfunction can be aggravated by shortening of diastolic phase (1,12,31). Tachycardia is also prone to induce myocardial ischemia even in HCM with angiographically normal coronary arteries. Although rapid pacing linearly increases coro...

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“…High levels of circulating ANF have been described during percutaneous transluminal coro nary angioplasty [10,11], as well as following dipyrida mole-dependent myocardial ischemia associated with a marked rise in ischemic regional wall stress [13]. In the latter study ANF was measured in a single blood sample at 'peak dipyridamole', and the patients were not studied under placebo infusion.…”

Section: Discussionmentioning

confidence: 99%

“…Atrial natriuretic factor (ANF) promotes diuresis and natriuresis, and interacts with the renin-angiotensin sys tem in experimental animal models and in man [1,2] whereas its role in the regulation of the peripheral vascu culating ANF was reported to rise after moycardial infarc tion [9] while little information is available on its levels during transient myocardial ischemia [10,11]. The dipy ridamole echocardiography test (DET) is used as screen ing procedure in patients with coronary artery disease (CAD): it causes an ischemia-induced reduction of region al left ventricular (LV) function with dyssynergy detect able by ultrasound [12].…”

Section: Introductionmentioning

confidence: 99%

Atrial Natriuretic Factor Release during Transient Myocardial Ischemia: A Placebo-Controlled Study in Man

Cassisa¹,

Tonolo²,

Glorioso³

et al. 1993

Am J Noninvas Cardiol

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Atrial natriuretic factor (ANF) exerts a vasodilatory effect on the coronary bed in myocardial ischemia. Besides wall stretch, ANF release can also be triggered by endothelin in experimental models. We studied the time course of ANF release and its relationship with endothelin during transient myocardial ischemia in man. Twelve patients subjected to the dipyridamole echocardiography test (DET) in a single-blind, randomly balanced, placebo-controlled setting were studied. Circulating ANF and endothelin were monitored during both dipyridamole and placebo. Dipyridamole caused left ventricular (LV) dyssynergy in 6 patients (group 1: multiple or isolated coronary artery stenosis) and acute left atrial dilation in 5 out of 6. In these 5 patients, a progressive rise of circulating ANF was found soon after LY dyssynergy, starting from time +8 min (55 ± 12 vs. 40 ± 7 at time 0 and 42 ± 8 pmol/1 time-matched placebo, p < 0.05 for both), becoming highly significantly different from + 10 min (72 ± 13 vs. 40 ± 7 at time 0 and vs. 47 ± 5 pmol/1 time-matched placebo, p < 0.01 for both) up to the end of the study (+40 min). Circulating ANF and echocardiographie parameters did not vary in the other 6 patients undergoing the DET (group 2) as well as during placebo in both groups. The DET caused heart rate and the rate-pressure products to increase to the same extent in both groups (+12 and +13%; +13 and +15%, respectively). Circulating endothelin did not vary. The consistent and long-lasting rise of circulating ANF in patients with coronary artery disease during transient myocardial ischemia indicate that ANF measurements during chest pain may be an important marker of the reduction in myocardial perfusion and LV dysfunction. Further studies will indicate if ANF may play a physiological role to attenuate anginal attacks.

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Plasma levels of atrial natriuretic peptide during myocardial ischemia induced by percutaneous transluminal coronary angioplasty or dynamic exercise

Cited by 28 publications

References 24 publications

Plasma amino‐terminal pro‐brain natriuretic peptide levels in subjects presenting to the Emergency Department with suspected acute coronary syndrome: possible role in selecting patients for follow up?

Plasma amino‐terminal pro‐brain natriuretic peptide levels in subjects presenting to the Emergency Department with suspected acute coronary syndrome: possible role in selecting patients for follow up?

Tachycardia-induced myocardial ischemia and diastolic dysfunction potentiate secretion of ANP, not BNP, in hypertrophic cardiomyopathy

Atrial Natriuretic Factor Release during Transient Myocardial Ischemia: A Placebo-Controlled Study in Man

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