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Quantification of left ventricular wall motion
ABSTRACTS
QUANTIFICATION OF LEFT VENTRICULAR WALL MOTION. Douglas K Stewart, MD; Harold T. Dodge, MD, FACC; Morris Frimer, MS., University of Washington, Seattle, Washington. A quantitative method for the study of segmental left ventricular (LV) wall motion throughout the cardiac cycle has been developed using biplane tine angiography in the antero-posterior and lateral projections at rates of 6080 frameslsec. Margins of the LV are traced on an X-Y digitizer and stored in a computer for playback and analysis. The system is programmed so that sequential frames are automatically aligned by superimposing the long axis of each silhouette permitting the normal displacement of the aortic valve. Local motion is described as wall movement toward the long axis as the percent of end diastolic dimension (EDD) along 10 hemiaxes for each plane. In 20 subjects with insignificant coronary disease wall motion of the basal 3/S of LV is greater for the anterior and lateral (57 to 68%) than for the inferior and septal walls (39 to 51%) and is completed earlier in systole (0.33 to 0.36 vs. 0.38 to 0.45 set). At the apical 2/S, wall motion of the inferior, anterior and lateral surfaces is similar in extent (59 to 88%) and timing. In 20 patients with ASHD abnormal wall segment motion has been classified by location, % shortening as compared to normal, time to maximum shortening, and the number of segments involved. 17 had hypokinetic or akinetic areas using the above normal standards and late contraction of such segments was common. Late contraction often occurred at a time when other segments were relaxing. These studies define a quantitative method of analyzing abnormal LV wall motion.
THE COST OF CARDIAC PACING William S. Stoney, MD, FACC; William C. Alford, MD, FACC; George R. Burrus, MD; and Jr., Clarence S. Thomas, Jr., MD, FACC. St. Thomas Hospital, Nashville, Tennessee. The patient with a permanent pacemaker faces continuous significant medical expenses for the remainder of his life. A review of the financial records of 15 patients paced for more than 4 years (average 73 months) was conducted to esEach tablish the basic monthlv cost of oacina. pacemaker was replaced alter 24 months of service. A total of 1096 paced months was reviewed which included 65 hospital admissions. The total hospital expense was $93,400 and the total physicians' fees was $18,750. The cost per month was calculated for each patient and varied from a low of $7l/month to a hiah of $129/month. The total expense for the"15 patients was $112,150 with an average cost per patient per month of $102. It was found that only one half of the total expense was recovered by the hospital. The patient paid 6% ($5,200) and Blue Cross or other insurance paid 5% ($4,600). Medicare paid a total of 38% ($35,600) leaving an unpaid balance of 51% ($47,900). This was written off as a reduction of revenue by the hospital as a medicare allowance. Permanent cardiac pacing increases the medical expenses of a patient by an average of $102 per month. Fortunately for the patient the majority of the expense is borne by Medicare or other agent. Unfortunately for the hospital a large portion of this expense is not recovered.
DETECTION OF ACUTE MYOCARDIAL INFARCTION IN PATIENTS WITH TECHNETIUM 99m GLUCOHPTONATE. H.W. Strauss, MD., Jacques Rouleau, MD.,D. Rossman, MD., Bertram Pitt, MD., Johns Hopkins Medical Institution, Baltimore, MD. Technetium 99m glucoheptonate (TG) has been found to be localized in areas of acutely infarcted myocardium in animals. TG was administered in doses of lo-15 millicuries to 13 patients between 5 and 48 hours after onset of chest pain. Scintiphotographs of the left chest were obtained between 30 minutes and 4 hours after injection in the right and left anterior oblique projection. Eight patients had definite ECG evidence of acute myocardial infarction on admission, the TG scan was positive in all. Five patients had equivocal evidence of acute myocardial infarction by ECG on admission, 2 had positive TG scans. Acute infarction was confirmed by serial ECG and creatinine phosphokinese (CPK) studies in these 2 patients. The remaining 3 patients had normal TG scans and did not prove to have acute myocardial infarction by serial ECG or CPK studies. In the 10 patients with serial ECG and CPK evidence of acute myocardial infarction there was a good correlation between peak CPK values and the % of the left ventricur = 0.91 P <.Ol (peak CPK lar area aCCUmUhting TG. range 86-2270units, % left ventricular area range 2164%). TG myocardial imaging is useful in the detection and estimation of the size of the acute myocardial infarction.
SERUM MYOGLOBIN LEVELS IN THE DIAGNOSIS OF MYOCARDIAL INFARCTION C. Bevan Stuart, MD; Fred J. Palmer, MD; Mr. Georse W. Nevatt: John E. Lewis, MD, PhD: Rov V. Juti?;, MD, FACC;.Jerald C. Nelson, MD, Loma Linda University Medical Center, Loma Linda, California. A recently developed radioimmunoassay for myoglobin was used to determine serum myoglobin levels in patients with myocardial infarction. Blood samples were obtained from patients immediately upon admission to hospital, hourly for the next 12 hours and then at 24 and 48 hours after the onset of chest pain. The presence of myocardial infarction was documented bv standard electrocardiosraohic and serum enzyme criteria. Serum myogiobin was undetectable in 23 control subjects. All 5 patients with acute myocardial infarction had myoglobinemia ranging from 46-200 ngm/ml in the first available specimen (4 to 7 hours after the onset of pain). The peak serum myoglobin concentration ranged from 152-880 ngm/ml and occurred at 7 to 10 hours after the onset of pain. On the other hand, the serum creatinine phosphokinase levels peaked at 17 to 33 hours. In 2 patients with severe chest pain without acute myocardial infarction, no serum myoglobin was detected. Thus, myoglobinemia is an earlier indicator of myocardial infarction than routine serum enzymes.
January 1975
The American Journal of CARDIOLOGY
Volume 35
171
QUANTIFICATION OF LEFT VENTRICULAR WALL MOTION. Douglas K Stewart, MD; Harold T. Dodge, MD, FACC; Morris Frimer, MS., University of Washington, Seattle, Washington. A quantitative method for the study of segmental left ventricular (LV) wall motion throughout the cardiac cycle has been developed using biplane tine angiography in the antero-posterior and lateral projections at rates of 6080 frameslsec. Margins of the LV are traced on an X-Y digitizer and stored in a computer for playback and analysis. The system is programmed so that sequential frames are automatically aligned by superimposing the long axis of each silhouette permitting the normal displacement of the aortic valve. Local motion is described as wall movement toward the long axis as the percent of end diastolic dimension (EDD) along 10 hemiaxes for each plane. In 20 subjects with insignificant coronary disease wall motion of the basal 3/S of LV is greater for the anterior and lateral (57 to 68%) than for the inferior and septal walls (39 to 51%) and is completed earlier in systole (0.33 to 0.36 vs. 0.38 to 0.45 set). At the apical 2/S, wall motion of the inferior, anterior and lateral surfaces is similar in extent (59 to 88%) and timing. In 20 patients with ASHD abnormal wall segment motion has been classified by location, % shortening as compared to normal, time to maximum shortening, and the number of segments involved. 17 had hypokinetic or akinetic areas using the above normal standards and late contraction of such segments was common. Late contraction often occurred at a time when other segments were relaxing. These studies define a quantitative method of analyzing abnormal LV wall motion.
THE COST OF CARDIAC PACING William S. Stoney, MD, FACC; William C. Alford, MD, FACC; George R. Burrus, MD; and Jr., Clarence S. Thomas, Jr., MD, FACC. St. Thomas Hospital, Nashville, Tennessee. The patient with a permanent pacemaker faces continuous significant medical expenses for the remainder of his life. A review of the financial records of 15 patients paced for more than 4 years (average 73 months) was conducted to esEach tablish the basic monthlv cost of oacina. pacemaker was replaced alter 24 months of service. A total of 1096 paced months was reviewed which included 65 hospital admissions. The total hospital expense was $93,400 and the total physicians' fees was $18,750. The cost per month was calculated for each patient and varied from a low of $7l/month to a hiah of $129/month. The total expense for the"15 patients was $112,150 with an average cost per patient per month of $102. It was found that only one half of the total expense was recovered by the hospital. The patient paid 6% ($5,200) and Blue Cross or other insurance paid 5% ($4,600). Medicare paid a total of 38% ($35,600) leaving an unpaid balance of 51% ($47,900). This was written off as a reduction of revenue by the hospital as a medicare allowance. Permanent cardiac pacing increases the medical expenses of a patient by an average of $102 per month. Fortunately for the patient the majority of the expense is borne by Medicare or other agent. Unfortunately for the hospital a large portion of this expense is not recovered.
DETECTION OF ACUTE MYOCARDIAL INFARCTION IN PATIENTS WITH TECHNETIUM 99m GLUCOHPTONATE. H.W. Strauss, MD., Jacques Rouleau, MD.,D. Rossman, MD., Bertram Pitt, MD., Johns Hopkins Medical Institution, Baltimore, MD. Technetium 99m glucoheptonate (TG) has been found to be localized in areas of acutely infarcted myocardium in animals. TG was administered in doses of lo-15 millicuries to 13 patients between 5 and 48 hours after onset of chest pain. Scintiphotographs of the left chest were obtained between 30 minutes and 4 hours after injection in the right and left anterior oblique projection. Eight patients had definite ECG evidence of acute myocardial infarction on admission, the TG scan was positive in all. Five patients had equivocal evidence of acute myocardial infarction by ECG on admission, 2 had positive TG scans. Acute infarction was confirmed by serial ECG and creatinine phosphokinese (CPK) studies in these 2 patients. The remaining 3 patients had normal TG scans and did not prove to have acute myocardial infarction by serial ECG or CPK studies. In the 10 patients with serial ECG and CPK evidence of acute myocardial infarction there was a good correlation between peak CPK values and the % of the left ventricur = 0.91 P <.Ol (peak CPK lar area aCCUmUhting TG. range 86-2270units, % left ventricular area range 2164%). TG myocardial imaging is useful in the detection and estimation of the size of the acute myocardial infarction.
SERUM MYOGLOBIN LEVELS IN THE DIAGNOSIS OF MYOCARDIAL INFARCTION C. Bevan Stuart, MD; Fred J. Palmer, MD; Mr. Georse W. Nevatt: John E. Lewis, MD, PhD: Rov V. Juti?;, MD, FACC;.Jerald C. Nelson, MD, Loma Linda University Medical Center, Loma Linda, California. A recently developed radioimmunoassay for myoglobin was used to determine serum myoglobin levels in patients with myocardial infarction. Blood samples were obtained from patients immediately upon admission to hospital, hourly for the next 12 hours and then at 24 and 48 hours after the onset of chest pain. The presence of myocardial infarction was documented bv standard electrocardiosraohic and serum enzyme criteria. Serum myogiobin was undetectable in 23 control subjects. All 5 patients with acute myocardial infarction had myoglobinemia ranging from 46-200 ngm/ml in the first available specimen (4 to 7 hours after the onset of pain). The peak serum myoglobin concentration ranged from 152-880 ngm/ml and occurred at 7 to 10 hours after the onset of pain. On the other hand, the serum creatinine phosphokinase levels peaked at 17 to 33 hours. In 2 patients with severe chest pain without acute myocardial infarction, no serum myoglobin was detected. Thus, myoglobinemia is an earlier indicator of myocardial infarction than routine serum enzymes.
January 1975
The American Journal of CARDIOLOGY
Volume 35
171