Unexplained atrial flutter: A frequent herald of pulmonary embolism
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Transcript of Unexplained atrial flutter: A frequent herald of pulmonary embolism
ABSTRACTS
crease pulmonary arterial pressure. Flow relat,ions through the anomalously and normally draining lobes are governed by total resistance to flow t’hrough respective lung segments, including resistance of respective lung vessels plus resistance to filling of respect.ive ventricles. Mit.ral tightening initially raises ventricular filling resistance and passively lowers resistance of normally draining vessels, without causing any change in total resistance through the normally draining lobes. As additional t’ightening raises total resistance through
The Ultrastructure of the His Bundle in the Dog
THOMAS N. JAMES, MD, FACC and LIB1 SHERF, MD, FACC Birmingham, Alabama
Compared to t.he detailed eleetrophysidlogic data available, little is known of the ultrastructure of the His bundle. This study was performed to examine the His bundle in 2 dogs
The cells of the His bundle are prolonged and organized
with electron microscopy. The technique has been published
in strands (two or three cells parallel) covered by collagen. The lateral intercellular margins contain both tight junctions
previously ( CirczUion, 34: 139, 1966).
and desmosomes. The ends of the cells do not form inter- calated discs; instead, “tongues” protrude into the next cell or in the interspace between two cells. The end-to-end margins contain desmosomes, and curve in smooth conti- nuity with the lateral aspect of the cell.
The cells are covered by a flat sarcolemma. The myo- fibrils are few, with sparse myofilaments, and often are not,
the normally draining lobe above that of the anomalously draining lobe, shunting increases. Provided the right ven- tricle remains competent, equilibrium is attained with high flow and low fixed total resistance in the anomalously drain- ing lobe and high tot,al resistance and fixed flow in the normally draining lobes. Although all lobes have the same degree of pulmonary arterial hypertension, the increased pulmonary venous hypertension causes selective vascular damage in the normally draining lobes.
parallel. Between myofibrils large empty spaces a.re ob- served. Numerous groups of mitochondria appear between myofibrils. Some His bundle cells appear to contain two
The fine structure of these specirtlized cells was compared to that of typical working myocardial cells in t.he septum.
nuclei. A Golgi apparatus is present. A variety of tubular
Working cells are darker, due to a greater number of myo- fibrils and myofilaments, with lack of empty spaces. Mito-
profiles are distributed at random.
chondria were sandwiched in single rows between myo- fibrils, and typical intercalated discs were present. The sarcolemma presented classic arca,des.
Both the structure of single cells and their organization within the His bundle are compatible with the function of rapid conduction, which is longitudinally partit,ioned.
Unexplained Atrial Flutter: A Frequent Herald of Pulmonary Embolism
JENNIFER C. JOHNSON, MD/NANCY C. FLOWERS, MD, FACC and LEO G. HORAN, MD, FACC Augusta, Georgia
Alt,hough it has been previously noted that atria1 arrhyth- mias may be associa.ted with puhnona.ry embolism, it has not been well appreciated that atria1 flutter with block may provide a strong hint to covert pulmonary embolism.
In 3,692 consecutive new patients studied in our laboratory after September 1967, 36 subjects with atria1 flutter were observed. The diagnosis of the arrhythmia was made possible in 6 instances in which esophageal leads were used to clarify the mechanism of regular rapid rhythms. Of the 36, 5 had definite postmortem demonstration of pulmonary embolism,
positive pulmonary angiograms or radioisotope lung scans. Nine had classic clinical findings of pulmonary embolism, and 6 had other active pulmonary disease. The remaining 16 were of diverse cause, including potential sources of embolism such as cardiomyopathy.
We suggest that (1) the findings of atria1 flutter without clearcut origin should alert the clinician to the possibility of hidden pulmonary embolism, and (2) the detection of atrial flutter with block can be enhanced by judicious resort to esophageal electrocardiography.
Direct Reconstruction of Flow to Small Distal Coronary Arteries
W. DUDLEY JOHNSON, MD/ROBERT J. FLEMMA, MD and DERWARD LEPLEY, Jr., MD, FACC Milwaukee, Wisconsin
During the past year immediate revascularization of the heart has been achieved in nearly all patients (97%) with the use of vein bypass grafts. Previous pathologic studies have shown the distal coronary arteries to be normal in most
pat,ients with ischemia. These findings have been confirmed clinically, and with our development of a system of fine ves- sel anastomoses, nearly all patients now can benefit from direct coronary surgery. Since July 1968, free vein grafts have been inserted into any coronary artery 11/2 to 2 mm
VOLUME 25, JANUARY 1970 105