Jack Sherez

Pulmonary venous flow pattern--its relationship to cardiac dynamics. A pulsed Doppler echocardiographic study.

We studied the physiology of pulmonary venous flow in 13 normal subjects and five patients with atrial rhythm disorders and atrioventricular conduction disturbances with pulsed Doppler and two-dimensional echocardiography. The left atrium, mitral valve, and pulmonary venous ostia were visualized through the apical four-chamber view. Mitral and pulmonary venous flows were obtained by placing the Doppler sample volume at the appropriate orifice. Pulmonary venous flow was biphasic: a rapid filling wave was observed during systole when the mitral valve was closed; a second wave was observed in diastole during the rapid ventricular filling phase of mitral flow, but was significantly delayed. In patients without atrial contraction (atrial fibrillation and sinoatrial standstill), the initial rapid filling was greatly diminished and only the second diastolic wave appeared to contribute to left atrial filling. In patients with high-grade atrioventricular block, each atrial contraction was followed by a surge in flow from the pulmonary veins. These results are consistent with data obtained from invasive measurements in both dogs and man, and confirm the validity of the use of pulsed Doppler echocardiography in the study of pulmonary venous flow. We suggest that pulmonary venous flow is influenced by dynamic changes in left atrial pressure created by contraction and relaxation of the atrium and ventricle. The initial peak in pulmonary venous flow occurs with atrial relaxation simultaneously with the reduction of left atrial pressure, and the second peak occurs with left ventricular relaxation and rapid transmitral filling of the ventricle.

Atrial contraction is an important determinant of pulmonary venous flow.

Pulmonary venous flow has two phases (systolic and diastolic) in normal subjects when studied by pulsed Doppler echocardiography. Only one phase of pulmonary venous flow (diastolic) was observed in six patients without synchronous atrial contraction (four patients with atrial fibrillation and two with complete atrioventricular [AV] block). This pattern reversed to normal (biphasic) when AV synchrony was reestablished by cardioversion to sinus rhythm in patients with atrial fibrillation and by AV sequential pacing in patients with complete AV block. Thus, both atrial and ventricular contraction and relaxation are important determinants of pulmonary venous flow.

Interrelationship of mid-diastolic mitral valve motion, pulmonary venous flow, and transmitral flow.

This study offers a unifying mechanism of left ventricular filling dynamics to link the unexplained mid-diastolic motion of the mitral valve with an associated increase in transmitral flow, with the phasic character of pulmonary vein flow, and with changes in the atrioventricular pressure difference. M mode echograms of mitral valve motion and Doppler echocardiograms of mitral and pulmonary vein flow velocities were recorded in 12 healthy volunteers (heart rate = 60 +/- 9 beats/min). All echocardiograms showed an undulation in the mitral valve (L motion) at a relatively constant delay from the peak of the diastolic phase of pulmonary vein flow (K phase). In six subjects, the L motion was also associated with a distinct wave of mitral flow (L wave). Measured from the onset of the QRS complex, Q-K was 577 +/- 39 msec; Q-L was 703 +/- 42 msec, and K-L was 125 +/- 16 msec. Multiple measurements within each subject during respiratory variations in RR interval indicated exceptionally small differences in the temporal relationships (mean coefficient of variation 2%). Early rapid flow deceleration is caused by a reversal of the atrioventricular pressure gradient, and the L wave arises from the subsequent reestablishment of a positive gradient due to left atrial filling via the pulmonary veins. The mitral valve moves passively in response to the flowing blood and the associated pressure difference. This interpretation is confirmed by (1) a computational model, and (2) a retrospective analysis of data from patients with mitral stenosis and from conscious dogs instrumented to measure transmitral pressure-flow relationships.

Atrial fibrillation and atrial enlargement in patients with mitral stenosis

The present study was designed to assess the relative contribution of atrial fibrillation and left atrial pressure to changes in the size of the left and right atria in patients with mitral stenosis. The study included 155 subjects, 102 of whom underwent prospective echocardiography and Doppler cardiography, and 69 of whom underwent cardiac catheterization. The size of the atria was determined by two-dimensional echocardiography. There were no significant hemodynamic differences between patients with mitral stenosis who were in either sinus rhythm or atrial fibrillation. The left atrium was larger (p less than 0.001) in patients with mitral stenosis and atrial fibrillation (37.6 +/- 10.8 cm2) than in patients in sinus rhythm (27.8 +/- 7.7 cm2) or normal subjects (15 +/- 3.3 cm2). The size of the right atrium was larger (p less than 0.001) in patients with mitral stenosis and atrial fibrillation (21.7 +/- 5.2 cm2) than in patients in sinus rhythm (13.4 +/- 3.9 cm2) or normal subjects (13.8 +/- 3.7 cm2). Multiple regression analysis showed that the severity of mitral stenosis accounted for 38%, age for 7%, and atrial fibrillation for 11% of the change in the size of the left atrium. Atrial fibrillation accounted for 24%, age for 11, and mitral valve area for 3% of the change in the size of the right atrium. The analysis suggests that the onset of left atrial dilatation in mitral stenosis is the result of an early increase in left atrial pressure. Atrial fibrillation, which develops irrespective of the severity of the mitral stenosis, contributes to a further enlargement of the left and right atria.

AORTIC DISSECTION MANIFESTED AS FEVER OF UNKNOWN ORIGIN

Aortic dissection is accompanied by fever in about one third of the patients. However, fever of unknown origin as the predominant manifestation of aortic dissection seems to be extremely rare. A review of the English literature revealed only 3 patients characterized by fever as the principal sign of aortic dissection. Herein an additional patient is reported. All 4 patients presented with pain or discomfort in the chest, back or abdomen, followed by persistent fever, lasting 5-11 weeks and associated with anemia and a high sedimentation rate. The outcome was favorable in all cases regardless of the location of the dissection or the type of treatment.

Tyrphostin AG-556 reduces myocardial infarct size and improves cardiac performance in the rat.

TNF-alpha is a proinflammatory cytokine, abundantly expressed after myocardial infarction. It has been suggested that it exhibits myocardial suppressive and cytotoxic effects. AG-556 is a tyrosine kinase inhibitor synthesized based on its ability to reduce TNF-alpha production and cell toxicity, and to improve experimental models mediated by TNF-alpha (i.e., peritontitis and experimental autoimmune encephalomyelitis). Daily, for 7 days, rats were injected ip with either AG-556 dissolved in DMSO or with the control vehicle. Infarct size was determined in the hearts as well as in fibrous scar formation. Cardiac TNF-alpha expression was evaluated by ELISA and immunohistochemistry. Functional hemodynamic parameters were evaluated employing echocardiography prior to sacrifice. AG-556 treatment reduced MI size at 7 days with a parallel effect on fibrous tissue formation. TNF-alpha production by splenocytes was reduced upon AG-556 treatment, whereas no differences were evident between the groups with regard to myocardial cytokine expression. AG-556 attenuated the decrease in fractional shortening at the expense of preserving end systolic diameter. AG-556 has proven beneficial in reducing myocardial infarct size and attenuated consequent hemodynamic deterioration in the rat model. If reconfirmed, AG-556 may be of potential clinical use in post-MI patients.

Discriminating Circulatory Problems From Deconditioning: Echocardiographic and Cardiopulmonary Exercise Test Analysis

Background: Discriminating circulatory problems with reduced stroke volume (SV) from deconditioning, in which the muscles cannot consume oxygen normally, by gas exchange parameters is difficult. Methods: We performed combined stress echocardiography (SE) and cardiopulmonary exercise tests (CPET) in 110 patients (20 with normal effort capacity, 54 with attenuated SV response, and 36 with deconditioning) to evaluate multiple hemodynamic parameters and oxygen content difference (A‐Symbolo2 Diff) in four predefined activity levels to assess which of the gas measures may help in the discrimination. Symbol. No caption available. Results: Reduced anaerobic threshold (AT), low unchanging peak oxygen pulse, periodic breathing, shallow &Dgr; peak oxygen consumption (Symbolo2)/&Dgr;work rate (WR) ratio, and high expired volume per unit time/carbon dioxide production (Symbole/Symbolco2) slope were all associated with abnormal SV response (P < .05 for all). The best discriminator was Symbole/Symbolco2 slope to Symbolo2 ratio (≥ 2.7; area under the curve [AUC], 0.79; P < .0001). The optimal gas exchange model included &Dgr;Symbolo2/&Dgr;WR < 8.6; Symbole/Symbolco2 slope to peak Symbolo2 ratio ≥ 2.7, and periodic breathing (AUC of 0.84; P < .0001). Symbol. No caption available. Symbol. No caption available. Symbol. No caption available. Symbol. No caption available. Symbol. No caption available. Symbol. No caption available. Symbol. No caption available. Symbol. No caption available. Symbol. No caption available. Symbol. No caption available. Conclusions: The best single gas exchange parameter to discriminate between circulatory problems and deconditioning is Symbole/Symbolco2 slope to peak SymbolO2 ratio. Combining it with &Dgr;Symbolo2/&Dgr;WR and periodic breathing improves the discriminative ability. Symbol. No caption available. Symbol. No caption available. Symbol. No caption available. Symbol. No caption available.

The New Editorial Board: 1991-1996

The New Editorial Board: 1991-1996 Cardiology was first published in 1937; the original editors were Drs. Bruno Kirsch of Cologne and W. Löffler of Zurich. The journal was originally named Cardiologia International Archives of Cardiology. In 1970, the name of the journal was changed to Cardiology. The Editorial Board at the time the journal was founded consisted of 24 distinguished cardiologists from Europe, North and South America, and Asia. The United States had 5 members including Paul D. White and Frank N. Wilson; Switzerland had 3 members, the UK and Czechoslovakia 2. The remaining 14 members came from the Netherlands, Portugal, Rumania, France, Germany, Sweden, Denmark, Austria, Mexico, and Japan. The 3 eastern European members are of even greater interest given current political changes in that region. More than half the articles in the first two volumes were in German, a quarter were in French, 15% were in Italian, and only 5% were in English. By 1960, the majority of the articles were in English, although French and German manuscripts were still being published. In 1970, when the journal took its present name, English became the sole language of the publication. Contributions in those first two volumes (1937-1938) came from the Netherlands, Italy, Germany, Denmark, France, Switzerland, and the USA. Each article ended with summaries in French, German, English, and Italian. There were no editorials and only occasional book reviews. Slightly more than one-third of the articles dealt with laboratory investigations in animals. Most studies were observational rather than experimental. It is interesting to review the topics covered in the first two volumes of Cardiologia. A number of animal studies were published including one of particular merit on the circulatory effects of intravenous epinephrine and adrenal cortical hormones. Clinical studies of note included work dealing with ventricular premature beats recorded by electrocardiography, congenital heart block, pathological observations on the etiology of atherosclerosis, and the application of cardiac output determinations to clinical problems. Thus, many of the topics which interest us today were already being considered in 1937 and 1938. Modern cardiology was already prefigured at that time. The new Editor and Editorial Board are honored to be part of a scholarly enterprise that is more than 50 years old. On behalf of the publisher and the members of the new Board, I would like to take a few minutes of 2 The New Editorial Board: 1991-1996