READERS’ COMMENTS Clarification
The article entitled “Termination of sustained ventricular tachycardia by external noninvasive pacing,” published in The American Journal of Cardiology in 1988 (61:574-577), of which I was the principal author, states that patients involved in that study gave informed written consent before electrophysiologic testing. That statement was incorrect, in that prior written consent was not obtained for all patients. All patients had, however, given prior oral consent, and I have now obtained written consents for all 8 participants who are living; the remaining 6 have unfortunately died. I did not obtain prior written consent because I incorrectly assumedthe external pacing to be an extension of their clinical care. The original data has been reviewed by Dr. David Leaman, the Medical Center’s Chief of Cardiology, and he finds no discrepancy with the published article aside from the matter mentioned above. I regret any inconvenience I have caused my colleagues or the Journal. Jerry C. Luck, MD
with multivessel coronary artery diseaseand previous myocardial infarction who probably had some left ventricular dysfunction at rest. In this study, all patients had normal left ventricular function in the control condition and had insignificant coronary lesions or l-vessel diseaseon coronary arteriography. Thus, the concept of diastolic dysfunction as a mechanism underlying impaired cardiac function is similar to the description of “backward failure” as originally proposedby Hope in 1832.2Similarly, “forward failure,” expounded in 1913 by MacKenzie,3 can be equated to systolic dysfunction. Although backward failure and forward failure hypotheses,2 seemingly opposite views that led to lively controversy during the first half of this century, were both later reconciled to be present in most patients with congestive heart failure, now, toward the end of this century, the pendulum once again swings in the direction whereby diastolic dysfunction can occur without systolic dysfunction. It is clinically important to distinguish diastolic dysfunction in coronary artery disease from systolic dysfunction, as the treatment is quite different.
Hershey, Pennsylvania 17 October 1990
Diastolic Dysfunction Prinzmetal’s Angina
in
Tsung 0. Cheng, MD
Washington, D.C. 14 November 1990 1. Doria E, Agostoni P, Loaldi A, Fiorentini C. Doppler assessmentof left ventricular filling pattern in silent ischemia in patients with Prinzmetal’s angina. Am J Cardiol 1990;66:1055-1059. 2. Hope J. A Treatise on the Diseases of the Heart and Great Vessels. London: Williams-Kidd, 1832. 3. McKenzie J. Diseases of the Heart, 3rd edition. London: Oxford University Press, 1913.
The elegant Doppler echocardiographic study of Doria et al’ confirms once again that left ventricular diastolic dysfunction can be not only a pure consequenceof myocardial ischemia but can also precede left ventricular systolic abnormalities. Their study differed from previous studies in that previous patient populations included subjects Role of Arterial Letters (from the United States) concerning a particular article in the Journal must be received within 2 months of the article’s publication, and should be limited (with rare exceptions) to 2 doublespaced typewritten pages. Two copies must be submitted.
Filters in the Prevention of Systemic Embolization by Microbubbles Released by Oxygenators
In a previous paper’ we reported our observations on the production of microbubbles by 2 different types of oxygenators during cardio-
pulmonary bypass (CPB). In that study, transesophageal echocardiography was used to detect microbubbles reaching the descending aorta in 20 patients undergoing various types of open-heart surgery. A hollow-fiber oxygenator was used in 10 patients and a bubble oxygenator in the remaining 10. An arterial filter was never used. When bubble oxygenators were used, microbubbles were seenas oblong bright particles with continuous, fast and circular movement in the descending aorta, throughout CPB. Conversely, with hollow-fiber oxygenators, the release of microbubbles was confined to the early phase of CPB, after the infusion of the priming solution. When commenting on our findings, we proposedthe incorporation of an arterial filter in the CPB circuit to “eliminate or significantly decreasethe number of oxygenatorgenerated microbubbles reaching the arterial circulation.” We therefore repeated the study in 2 more groups of 10 patients each, using exactly the same methodology and adding an arterial filter of proven efficacy (Pall Ultipor EC 3840) to the circuit.2 As expected, we found a great reduction in the number and the size of the microbubbles, which, however, still appearedconsistently and had an identical time-course as in the previous study. Specifically, they lasted throughout CPB when bubble oxygenators were used, and disappearedwithin 2 minutes when hollow-fiber oxygenators were used. These results are justified by the characteristics of the 40-ym filters that we used, which allow very small bubbles through, and by the high resolution of the transesophageal probe, permitting their detection. Our experience confirms data obtained with microbubble activity monitors3 and with transcranial Doppler probes,4which also show a significant reduction in the number and size of microbubbles when arterial filters are used. Although not resolute, arterial filters of the type we used seem helpful in decreasing gaseous microembolism in the systemic circu-
THE AMERICAN JOURNAL OF CARDIOLOGY APRIL 15, 1991
911
The article entitled “Termination of sustained ventricular tachycardia by external noninvasive pacing,” published in The American Journal of Cardiology in 1988 (61:574-577), of which I was the principal author, states that patients involved in that study gave informed written consent before electrophysiologic testing. That statement was incorrect, in that prior written consent was not obtained for all patients. All patients had, however, given prior oral consent, and I have now obtained written consents for all 8 participants who are living; the remaining 6 have unfortunately died. I did not obtain prior written consent because I incorrectly assumedthe external pacing to be an extension of their clinical care. The original data has been reviewed by Dr. David Leaman, the Medical Center’s Chief of Cardiology, and he finds no discrepancy with the published article aside from the matter mentioned above. I regret any inconvenience I have caused my colleagues or the Journal. Jerry C. Luck, MD
with multivessel coronary artery diseaseand previous myocardial infarction who probably had some left ventricular dysfunction at rest. In this study, all patients had normal left ventricular function in the control condition and had insignificant coronary lesions or l-vessel diseaseon coronary arteriography. Thus, the concept of diastolic dysfunction as a mechanism underlying impaired cardiac function is similar to the description of “backward failure” as originally proposedby Hope in 1832.2Similarly, “forward failure,” expounded in 1913 by MacKenzie,3 can be equated to systolic dysfunction. Although backward failure and forward failure hypotheses,2 seemingly opposite views that led to lively controversy during the first half of this century, were both later reconciled to be present in most patients with congestive heart failure, now, toward the end of this century, the pendulum once again swings in the direction whereby diastolic dysfunction can occur without systolic dysfunction. It is clinically important to distinguish diastolic dysfunction in coronary artery disease from systolic dysfunction, as the treatment is quite different.
Hershey, Pennsylvania 17 October 1990
Diastolic Dysfunction Prinzmetal’s Angina
in
Tsung 0. Cheng, MD
Washington, D.C. 14 November 1990 1. Doria E, Agostoni P, Loaldi A, Fiorentini C. Doppler assessmentof left ventricular filling pattern in silent ischemia in patients with Prinzmetal’s angina. Am J Cardiol 1990;66:1055-1059. 2. Hope J. A Treatise on the Diseases of the Heart and Great Vessels. London: Williams-Kidd, 1832. 3. McKenzie J. Diseases of the Heart, 3rd edition. London: Oxford University Press, 1913.
The elegant Doppler echocardiographic study of Doria et al’ confirms once again that left ventricular diastolic dysfunction can be not only a pure consequenceof myocardial ischemia but can also precede left ventricular systolic abnormalities. Their study differed from previous studies in that previous patient populations included subjects Role of Arterial Letters (from the United States) concerning a particular article in the Journal must be received within 2 months of the article’s publication, and should be limited (with rare exceptions) to 2 doublespaced typewritten pages. Two copies must be submitted.
Filters in the Prevention of Systemic Embolization by Microbubbles Released by Oxygenators
In a previous paper’ we reported our observations on the production of microbubbles by 2 different types of oxygenators during cardio-
pulmonary bypass (CPB). In that study, transesophageal echocardiography was used to detect microbubbles reaching the descending aorta in 20 patients undergoing various types of open-heart surgery. A hollow-fiber oxygenator was used in 10 patients and a bubble oxygenator in the remaining 10. An arterial filter was never used. When bubble oxygenators were used, microbubbles were seenas oblong bright particles with continuous, fast and circular movement in the descending aorta, throughout CPB. Conversely, with hollow-fiber oxygenators, the release of microbubbles was confined to the early phase of CPB, after the infusion of the priming solution. When commenting on our findings, we proposedthe incorporation of an arterial filter in the CPB circuit to “eliminate or significantly decreasethe number of oxygenatorgenerated microbubbles reaching the arterial circulation.” We therefore repeated the study in 2 more groups of 10 patients each, using exactly the same methodology and adding an arterial filter of proven efficacy (Pall Ultipor EC 3840) to the circuit.2 As expected, we found a great reduction in the number and the size of the microbubbles, which, however, still appearedconsistently and had an identical time-course as in the previous study. Specifically, they lasted throughout CPB when bubble oxygenators were used, and disappearedwithin 2 minutes when hollow-fiber oxygenators were used. These results are justified by the characteristics of the 40-ym filters that we used, which allow very small bubbles through, and by the high resolution of the transesophageal probe, permitting their detection. Our experience confirms data obtained with microbubble activity monitors3 and with transcranial Doppler probes,4which also show a significant reduction in the number and size of microbubbles when arterial filters are used. Although not resolute, arterial filters of the type we used seem helpful in decreasing gaseous microembolism in the systemic circu-
THE AMERICAN JOURNAL OF CARDIOLOGY APRIL 15, 1991
911
