ANF rise during PTCA

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letters

to the

June 1993 American Heart Journal

Editor

0.78 = 1.74, a duration which is 1.72 seconds.

REPLY To the Editor: We thank Drs. Tomcs&nyi and Tenczer for their interest in our paper. Their comment on variability of postextrasystolic pauses is absolutely correct. The phenomenon had already been noted by us. but it was not mentioned because it was not related to the main topic of the paper. The tracing reported by us reflects extremely variable postextrasystolic pauses. The sinus PP interval containing the extrasystolic P wave, indeed, ranges from 1.52 seconds to 1.84 seconds (Fig. 1) even though the coupling intervals of premature P waves are not widely variable. Analysis of the tracing reveals that such pause variability is not the result of discharge or depression of the sinus pacemaker by ectopic impulses, but mere11 depends on sinus arrhythmia. This theory is suggested from the variability of sinus PP intervals that range from 0.76 seconds to 1 .O seconds (Fig. 1). It should be pointed out that PP interval prolongation is not a result of postdischarge sinus node depression: indeed, in the second strip the PP interval lengthens up to 0.96 set before the extrasystole. This establishes that PP interval variability is the result of spontaneous sinus cycle fluctuation, independent of sinus node passive discharge. Therefore any postextrasystolic pause should be considered compensatory even though the long sinus PP interval encompassing the premature ectopic impulse is not exactly corresponding to the sum of the sinus PP intervals that precede and follow the extrasystole. The first pause is clearly compensatory because it measures 1.52 set; the sum of the preceding plus the following PP int.erval is 1.55 sec. The second pause (1.84 set) appears as less than compensatory because the sum of the preceding plus the following PP interval is 1.96 sec. It may be assumed, however, that the pause of 1.84 seconds results from 2 cycles of 0.92 seconds, a reasonable assumption provided that the sinus cycle is variable, with the interval of 0.96 seconds being preceded by an interval of 0.80 seconds, whereas the interval of 1.0 seconds is followed by an interval of 0.92 seconds. Both the third and the fourth pauses are exactly compensatory because 1.69 = 0.89 + 0.80 and 0.96 +

Fig.

1. A continuous recording of lead VI. Dots low the tracing express PR intervals, and numbers time intervals are in hundredths of a second.

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Giusepp? Oreto. MI) Francesco l~zzn, MI) Gaetano Satullo, MI) Ant~t~ino Donalo, MIJ Ignazio M. Scimonr, Mli Maria Pia (Jalahro, Ml) Via Terranoun. 9 98122 Messina Itnl? 418/45849

ANF RISE DURING PTCA To the Editor: Malatino et al.’ demonstrated a significant increase of atria1 natriuretic factor (ANF) of pulmonary arterial blood during percutaneous transluminal coronary angioplasty (PTCA); they also demonstrated that the changes of ANF correlated with changes of pulmonary capillary wedge pressure (PCWP) levels. Their results agree with our report,2 in which we found remarkably higher concentrations of venous and pulmonary arterial ANF during PTCA in patients with increased PCWP compared with patients whose PCWP level did not significantly rise. ANF concentrations correlated with PCWP levels. Malatino et al.’ conclude that transient myocardial ischemia that results from PTCA stimulates ANF release; however, they give no evidence of ischemia in their patients. In all of our patients in whom PCWP and ANF increased, angina1 pain and ischemic electrocardiographic changes occurred during PTCA, only 3 of 10 patients without significant changes of PCWP and ANF had signs of myocardial ischemia. We postulated that the cause for the increase of ANF was ischemic left ventricular dysfunction with concomitant increase in left atria1 pressure and wall distension and possibly not the myocardial ischemia per se.

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Volume 125, Number 6 American Heart Journal

Letters

Recently we found by measuring ANF and lactate concentrations from the coronary sinus and femoral artery that during PTCA the arteriovenous ANF difference increases only in those patients in whom the lactate extraction ratio decreases, reflecting a real metabolic ischemia (unpublished findings). Apparently, measurement of arteriovenous ANF difference by using blood samples from the coronary sinus is more accurate to show minor increases in ANF release and thus reveals whether minor myocardial ischemia causes increase in ANF secretion without concomitant increase in atria1 pressure, which has been found in animal studies.”

Oulu

1. Malatino LS, Leonardi C, Stancanelli B, Polizzi G, Grassi R, Tamburino C. Tamburino G. Transient mvocardial &hernia stimulates a&al natriuretic factor release. AM HEART J 1992;123:693-703. 2. Iklheimo MJ, Ruskoaho HJ, Airaksinen KEJ, Huikuri HV, Korhonen UR. Leanliluoto PJ. Tuominen MO. Takkunen JT. Plasma levels bf at&al natriuretic peptide duiing myocardial ischemia induced by percutaneous transluminal coronary angioplasty or dynamic-exercise. AM HEART J 1989;117:837-41. 3. Uusimaa PA. Peuhkurinen KJ. Hassinen IE. Vuolteenaho 0. Ruskoaho HI Ischemia stimulates the release of atria1 natri: uretic peptide from rat cardiac ventricular myocardium. Life Sci 1992;50:365-73. 4/8/45827

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artery) to assessarteriovenous differences in ANF levels. However, it has recently been shown that the ventricle is a major site of synthesis and secretion of another cardiac natriuretic hormone, brain natriuretic peptide (BNP); ANF is mainly synthesized in and released from the atrium.3 Bearing these findings in mind, the assessment of arteriovenous differences of BNP might help better evaluate the direct influence, if any, of ventricle ischemia on the release of natriuretic hormones. Lorenzo Malatino, MD Medica “L. Condorelli” Uniuersitk di Catania c/o Ospedale Vittorio Emanuele Via Plebiscite 628 I-95124 Cat&a

Istituto

di Clinica

Markku J. Ikiiheimo, MD Division of Cardiology Department of Medicine University Central Hospital SF-90220 Oh, Finland

REFERENCES

to the Editor

Italy REFERENCES

1. Malatino LS, Leonardi C, Stancanelli B, Polizzi G, Grassi R, Tamburino C. Tamburino G. Transient mvocardial ischemia stimulates atria1 natriuretic factor release. "AM HEART J 1992; 123:693-8. 2. Ikaheimo MJ, Ruskoaho HJ, Airaksinen KEJ, Huikuri HV, Korhonen UR, LeppZiluoto PJ, Tuominen MO, Takkunen JT. Plasma levels of atria1 natriuretic peptide during myocardial &hernia induced by percutaneous transluminal coronary angioplasty or dynamic exercise. AM HEART J 1989;117:837-41. 3. Ogawa Y, Nakao K, Mukoyama K, Shirakami G, Arai H, Saito Y, Suga S, Jougasaki M, Imura H. Natriuretic peptides as cardiac hormones in normotensive and spontaneously hypertensive rats. The ventricle is a major site of synthesis and secretion of brain natriuretic peptide. Circ Res 1991;69:491-500. 4/8/45836

REPLY To The

Editor:

Dr. Iklheimo points out that our report,’ in which we found that the significant increase in atria1 natriuretic factor (ANF) levels detected in pulmonary arterial blood during percutaneous transluminal coronary angioplasty (PTCA) was closely related to changes in pulmonary capillary wedge pressure (PCWP) levels, agrees with previous findings by his group.2 As clearly stated at the beginning of our article,l and in agreement with Iklheimo et a1.,2 we believe that the close relationship between changes in ANF and PCWP during PTCA implies that transient modifications in cardiac function caused by acute myocardial ischemia could be involved in eliciting ANF release. In our group of patients undergoing PTCA, 10 of 11 had electrocardiographic (ECG) signs of ischemia during PTCA; among these 10 patients, 7 had symptoms of angina. All 10 patients showed a consistent increase in both ANF and PCWP; in the patient with neither ECG signs of &hernia nor angina only a weak change in both ANF and PCWP was observed. However, the hypothesis that myocardial &hernia itself can directly trigger ANF release may be warranted by the increase of venous levels of ANF associated with spontaneous angina.’ I believe that simultaneous measurements of lactate extraction ratio, as was recently done by Ikliheimo et al. (unpublished data) can provide metabolic evidence of myocardial &hernia, thereby establishing whether ischemia per se is capable of stimulating ANF release directly. Such an approach implies blood sampling to be simultaneously done in the coronary sinus and aorta (or femoral

LEFT ATRIAL

BALL THROMBUS

To the Editor:

In their report Kuo et a1.l state that left atria1 ball thrombi have never been reported in patients without rheumatic heart disease. However, at least one case of nonrheumatic left atria1 ball thrombus has been reported previously. In our recent review of this topic’ we mentioned a patient originally referred to by Read et a1.,3 who was found at necropsy to have a 3.5 cm x 5.0 cm, egg-shaped, unattached thrombus in the dilated left atrium. Before death this patient’s symptoms and physical examination findings were consistent with a diagnosis of left atria1 ball thrombus. He had no history of rheumatic or scarlet fever but was in atria1 fibrillation during his last hospitalization. Additional postmortem findings included biventricular hypertrophy (heart weight, 900 gm) and normal valves. The patient described by Kuo et al.’ is of interest because of the unusual presentation of a rare entity. The authors’ statement about the utility of transesophageal echocardiography in the diagnosis of left atria1 ball thrombus is well taken and is in accordance with comments made in our review. State University

of

David Wrisley, MD Alessandro Giambartolomei, MD New York Health Science Center 5100 W. Tuft Rd., Suite W

Syracuse, NY 13088