-type (atrial) natriuretic peptide (ANP) and B-type (brain) natriuretic peptide (BNP) are hormones with a wide range of potent biological effects, including natriuresis, diuresis, vasodilatation, and inhibition of the renin -angiotensin -aldosterone and sympathetic nervous systems. 1,2 We and others have shown that ANP is mainly synthesized and secreted from the atria in adult mammals, 1,3-5 but it is also synthesized and secreted from the ventricles in patients with congestive heart failure. [3][4][5] BNP is secreted mainly from the ventricles in normal adult humans as well as in patients with congestive heart failure, and the plasma concentrations of BNP are markedly increased in proportion to the severity of left ventricular (LV) dysfunction in patients with myocardial infarction (MI) or congestive heart failure. 4,[6][7][8] Plasma concentrations of ANP and BNP have been used to predict prognosis after MI. 8,9 It is widely accepted that asymptomatic post-MI patients have a high risk of progression to overt heart failure and death, 10 so it is clinically important to prevent their transition to a stage of accelerated progression of LV dysfunction. BNP concentrations are used to assess prognosis and therapeutic effects in asymptomatic MI patients as well as symptomatic patients 8,11 and the expression of both ANP and BNP is increased in the localized myocardial infarct regions relative to the detrimental hemodynamic parameters in patients with MI. 3,4,6,12 The increase in ANP and BNP concentrations precedes the development of symptoms in asymptomatic MI patients, 4,8,11 but it is unknown what determines the plasma concentrations of ANP and BNP in asymptomatic MI patients with relatively preserved LV function. Therefore, the present study was designed to examine whether the plasma concentrations of ANP and BNP serve as a clinical indicator of the extent of MI, an important determinant of mortality. 13 For these purposes we examined the relationship of plasma concentrations of ANP and BNP with the infarct size quantitatively calculated with thallium-201 single photon emission computed tomography (SPECT), a noninvasive and accurate method of assessment during the chronic phase of MI.

Background: The existence of atypical fast-slow (F/S) atrioventricular (AV) nodal reentrant tachycardias (NRT) using slow pathway (SP) variants connected to the right atrial (RA) inferolateral (inf) free wall (FW) along the tricuspid annulus (TA), has been neither confirmed nor precisely characterized. Methods and Results: We studied 7 patients (mean age, 48±16 years; 5 men) with F/S-AVNRT with long RP intervals and an earliest atrial activation at the RA inf-FW along the TA (inf-F/S-AVNRT). AV reentrant tachycardia was excluded on observation of the transition zone criteria in all 7 patients. Atrial tachycardia was excluded on the observation of a V-A-V activation sequence after the induction or entrainment of the tachycardia from the right ventricle in all. During the tachycardia, low-frequency, fractionated potentials (LP) preceding the local atrial electrogram were recorded near the site of the earliest atrial activation in 6 patients. Observations of conduction delay and block of the LP during ventricular entrainment or ablation of the tachycardia indicated that LP reflect retrograde activation via the inf-SP. Retrograde SP conduction was interrupted at the site of earliest atrial activation in 3 patients, and in the right posterior septum in 4 patients. Conclusions: inf-F/S-AVNRT are distinct supraventricular tachycardia incorporating an SP variant connected to the RA inf-FW along the TA in the retrograde direction, which were eliminated by ablation.

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