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Early revascularization in acute infarction, help or hazard: A randomized study
ABSTRACTS
THE EFFECT OF SYSTEMIC ARTERIAL PRESSURE ON COLLATERAL CORONARY FLOW IN MAN. Peter R. Maroko, MD; Lawrence H. Cohn, MD, FACC, Dept Med & Surg, Harvard Med Sch & Peter Bent Brigham Hosp, Boston, MA. The survival of myocardium in the area supplied by an occluded coronary artery depends on the quantity of blood delivered from the adjacent arteries through collaterals and is a function of the richness of the collateral network. However, it is not known how changes in arterial pressure (AP) can affect this collateral coronary flow (CCF) in patients. The methods used to measure CCF in man have been necessarily indirect. However, in patients undergoing aorto-coronary bypass a unique opportunity exists to measure directly the retrograde coronary flow, and the influence of changes in AP. Accordingly, in 6 patients, following the suture of the venous graft to the coronary artery, and before its connection to the aorta, an 18-gauge intracath was placed in the venous graft and the retrograde flow determined directly in a graduated cylinder. AP was raised from 45 to 115mmHg by altering flow in the heart-lung machine from 1000 to 450Oml/min. An increase in AP from 65 to 85mmHg induced an increase in CCF from 16.222.2 to 23.2?4.8mlfmin (px.01). Thus, an increase in 2OmmHg of AP augmented CCF by 48%. One patient showed no CCF and developed a nonfatal infarction postoperative. It is concluded that in each individual the quantity of blood supplied to an ischemic area through collaterals is not only dependent upon the number of collaterals but also upon arterial pressure, thus the latter may play a role in determining the amount of tissue which survives or evolves to necrosis following coronary occlusion.
ULTRASTRUCTURAL FEATURES OF CARDIAC MUSCLE CELLS IN LEFT VENTRICULAR MYOCARDIUM OF PATIENTS WITH CHRONIC AORTIC VALVULAR DISEASE. Barry J. Maron, MD; Victor J. Ferrans, MD; and William C. Roberts, MD, NHLI, Bethesda, Md. There is no information available on the ultrastructure of ventricular muscle cells of living pts with chronic aortic valvular disease. Therefore, apical left ventricular myocardium was resected at operation from 19 pts with aortic valvular disease and examined by light and electron microscopy. In 10 pts (6 with aortic stenosis, 4 with aortic regurgitation) only hypertrophied cardiac muscle cells and small amounts of interstitial fibrosis were present. In muscle from the other 9 pts (all with aortic regurgitation), however, both hypertrophied and degenerated cardiac muscle cells were observed. Hypertrophied cells demonstrated enlarged nuclei and increased numbers of normally appearing myofibrils, mitochondria, and ribosomes. Most degenerated cells were normal-sized, surrounded by large amounts of interstitial fibrosis and often had lost their connections with adjacent cells. These cells showed loss of normal myofibrillar structure with markedly reduced numbers of thick (myosin) filaments, streaming and clumping of Z band material and disorganization of thin (actin) filaments. The most severely degenerated muscle cells were atrophic with a few or no intact myofibrils. It is concluded that these alterations in the structure of Z bands and myofibrils reflect a degenerative process which probably results from the inability of certain hypertrophied cardiac muscle cells to meet functional demands imposed upon them, Furthermore, these degenerated cardiac muscle cells may be partly responsible for impaired myocardial function in pts with chronic valvular heart disease, left ventricular volume overloading, and congestive heart failure.
156
January 1974
The American Journal of CARDIOLOGY
EARLY REVASCULARIZATION IN ACUTE INFARCTION, HELP OR HAZARD: A RANDOMIZED STUDY Virendra S. Mathur, M.D., GeneA. Guinn, M.D., Baylor College of Medicine and VA Hospital, Houston, Texas Recently myocardial revascularization (REVAS) has been advocated in very early stages of acute infarction (MI)to reduce infarct size and complications. The role of maximal REVAS by restoring normal blood supply 2 hours (H) after MI was tested in conscious intact dogs. A previously implanted balloon-cuff around left anterior descending was inflated to produce MI and amongst the survivors it was left inflated in 13 controls (C) for 7 days, it was
deflated 2 H following MI in 17. Some of the results of serial studies of LV pressure, its peak dp/dt and dp/dt at developed pressure of 40 mmHg(dp/dt-4O),stroke work (SW),ejection fraction (EF) and myocardial 02 and lactate (L) extraction (EXTR) are tabulated (mea$SEM). CONTROL REVAS 3H 2H 7 28 16+2 17+3 16+2 15+2 LVedp mmHg 1872 Peak dp/dtxlO-2 1972 19?3 2573 1672 1773 2173 1672 dp/dt-40x10-2 692 742 76?5 9777 SW g.m. 462 4473 4774 463 EF % 73?2 7072 6513 71T3 02EXTR % 19z3 1573 113 la5 L EXTR % Differences between C and REVAS dogs were not significant. Ventricular tachycardia (VT) and dyskinesis developed and persisted in each C and REVAS dog and 23% C(3of 13) and 18% REVAS (3of17) died. The average infarct size was .29 of LV in C, larger (.36 of LV) in 6 of 17 REVAS dogs and smaller (.08 of LV) in 11 of 17 REVAS dogs. Conclusion:Early REVAS fails to prevent VT,death and hemo dynamic,metabolic and angiographic deterioration in acute canine MI and REVAS increases infarct size in one-third.
REVERSIBILITY OF LEFT VENTRICULAR ASYNERGY ASSESSED BY POST-NITROGLYCERIN LEFT VENTRICULOGRAPHY. Robert G. Matthews, MD; Sudhakar P. Reddy, MD; James D. O'Toole, MD; Rosemarie Salerni, MD; James A. Shaver, MD, University of Pittsburgh, Pittsburgh, Pennsylvania Left ventricular (LV) angiograms were performed before and after sublingual trinitroglycerin (TNG=0.4 mg) in 22 patients (pts) during routine cardiac catheterization for evaluation of coronary artery disease (CAD). Five pts had no organic heart disease (N). Seventeen pts had CAD vith LV dysfunction in the .first angio ram; 5 of them had previous myocardial infarction (MI4 , and 12 of them had angina (AN) alone. Basal (A), mid (B), apical (C) minor axes were measured from LV angiograms. Percentage systolic shortening (PSS) and change in PSS with TNG were calculated for each axis. The results for Group N were as follows: Percentage Systolic Shortening Change in PSS with TNG Mean SD+ Range (PSS) Mean SD+ Range A 48.3 -0.4 3.3 (45 to 55) 2.8 (-5 to +ll) B 38.2 8.7 (30 to ti3) 13.2 6.6 (+6 to +24) C 48.4 16.5 (38 to 81) 10.25 5.6 (-5 to +571 Less than 40, 30, and 3!; PSS was defined as asynergy and increase in PSS of more than 5, 20, and 25 with TNG was defined as supernormal response for A, B, and C Five MI pts had 14 asynergetic axes and respectively. did not change with TNG. There were 24 asynergetic axes in 12 AN pts; 8 showed normal and 16 supernormal response to TNG. In 4 AN pts reversal of asynergy was total and complete with TNG. Thus, the post-nitroglycerin left ventriculography is a simple, safe, and useful test to assess the reversibility of left ventricular asynergy in pts with CAD.
Volume 33
THE EFFECT OF SYSTEMIC ARTERIAL PRESSURE ON COLLATERAL CORONARY FLOW IN MAN. Peter R. Maroko, MD; Lawrence H. Cohn, MD, FACC, Dept Med & Surg, Harvard Med Sch & Peter Bent Brigham Hosp, Boston, MA. The survival of myocardium in the area supplied by an occluded coronary artery depends on the quantity of blood delivered from the adjacent arteries through collaterals and is a function of the richness of the collateral network. However, it is not known how changes in arterial pressure (AP) can affect this collateral coronary flow (CCF) in patients. The methods used to measure CCF in man have been necessarily indirect. However, in patients undergoing aorto-coronary bypass a unique opportunity exists to measure directly the retrograde coronary flow, and the influence of changes in AP. Accordingly, in 6 patients, following the suture of the venous graft to the coronary artery, and before its connection to the aorta, an 18-gauge intracath was placed in the venous graft and the retrograde flow determined directly in a graduated cylinder. AP was raised from 45 to 115mmHg by altering flow in the heart-lung machine from 1000 to 450Oml/min. An increase in AP from 65 to 85mmHg induced an increase in CCF from 16.222.2 to 23.2?4.8mlfmin (px.01). Thus, an increase in 2OmmHg of AP augmented CCF by 48%. One patient showed no CCF and developed a nonfatal infarction postoperative. It is concluded that in each individual the quantity of blood supplied to an ischemic area through collaterals is not only dependent upon the number of collaterals but also upon arterial pressure, thus the latter may play a role in determining the amount of tissue which survives or evolves to necrosis following coronary occlusion.
ULTRASTRUCTURAL FEATURES OF CARDIAC MUSCLE CELLS IN LEFT VENTRICULAR MYOCARDIUM OF PATIENTS WITH CHRONIC AORTIC VALVULAR DISEASE. Barry J. Maron, MD; Victor J. Ferrans, MD; and William C. Roberts, MD, NHLI, Bethesda, Md. There is no information available on the ultrastructure of ventricular muscle cells of living pts with chronic aortic valvular disease. Therefore, apical left ventricular myocardium was resected at operation from 19 pts with aortic valvular disease and examined by light and electron microscopy. In 10 pts (6 with aortic stenosis, 4 with aortic regurgitation) only hypertrophied cardiac muscle cells and small amounts of interstitial fibrosis were present. In muscle from the other 9 pts (all with aortic regurgitation), however, both hypertrophied and degenerated cardiac muscle cells were observed. Hypertrophied cells demonstrated enlarged nuclei and increased numbers of normally appearing myofibrils, mitochondria, and ribosomes. Most degenerated cells were normal-sized, surrounded by large amounts of interstitial fibrosis and often had lost their connections with adjacent cells. These cells showed loss of normal myofibrillar structure with markedly reduced numbers of thick (myosin) filaments, streaming and clumping of Z band material and disorganization of thin (actin) filaments. The most severely degenerated muscle cells were atrophic with a few or no intact myofibrils. It is concluded that these alterations in the structure of Z bands and myofibrils reflect a degenerative process which probably results from the inability of certain hypertrophied cardiac muscle cells to meet functional demands imposed upon them, Furthermore, these degenerated cardiac muscle cells may be partly responsible for impaired myocardial function in pts with chronic valvular heart disease, left ventricular volume overloading, and congestive heart failure.
156
January 1974
The American Journal of CARDIOLOGY
EARLY REVASCULARIZATION IN ACUTE INFARCTION, HELP OR HAZARD: A RANDOMIZED STUDY Virendra S. Mathur, M.D., GeneA. Guinn, M.D., Baylor College of Medicine and VA Hospital, Houston, Texas Recently myocardial revascularization (REVAS) has been advocated in very early stages of acute infarction (MI)to reduce infarct size and complications. The role of maximal REVAS by restoring normal blood supply 2 hours (H) after MI was tested in conscious intact dogs. A previously implanted balloon-cuff around left anterior descending was inflated to produce MI and amongst the survivors it was left inflated in 13 controls (C) for 7 days, it was
deflated 2 H following MI in 17. Some of the results of serial studies of LV pressure, its peak dp/dt and dp/dt at developed pressure of 40 mmHg(dp/dt-4O),stroke work (SW),ejection fraction (EF) and myocardial 02 and lactate (L) extraction (EXTR) are tabulated (mea$SEM). CONTROL REVAS 3H 2H 7 28 16+2 17+3 16+2 15+2 LVedp mmHg 1872 Peak dp/dtxlO-2 1972 19?3 2573 1672 1773 2173 1672 dp/dt-40x10-2 692 742 76?5 9777 SW g.m. 462 4473 4774 463 EF % 73?2 7072 6513 71T3 02EXTR % 19z3 1573 113 la5 L EXTR % Differences between C and REVAS dogs were not significant. Ventricular tachycardia (VT) and dyskinesis developed and persisted in each C and REVAS dog and 23% C(3of 13) and 18% REVAS (3of17) died. The average infarct size was .29 of LV in C, larger (.36 of LV) in 6 of 17 REVAS dogs and smaller (.08 of LV) in 11 of 17 REVAS dogs. Conclusion:Early REVAS fails to prevent VT,death and hemo dynamic,metabolic and angiographic deterioration in acute canine MI and REVAS increases infarct size in one-third.
REVERSIBILITY OF LEFT VENTRICULAR ASYNERGY ASSESSED BY POST-NITROGLYCERIN LEFT VENTRICULOGRAPHY. Robert G. Matthews, MD; Sudhakar P. Reddy, MD; James D. O'Toole, MD; Rosemarie Salerni, MD; James A. Shaver, MD, University of Pittsburgh, Pittsburgh, Pennsylvania Left ventricular (LV) angiograms were performed before and after sublingual trinitroglycerin (TNG=0.4 mg) in 22 patients (pts) during routine cardiac catheterization for evaluation of coronary artery disease (CAD). Five pts had no organic heart disease (N). Seventeen pts had CAD vith LV dysfunction in the .first angio ram; 5 of them had previous myocardial infarction (MI4 , and 12 of them had angina (AN) alone. Basal (A), mid (B), apical (C) minor axes were measured from LV angiograms. Percentage systolic shortening (PSS) and change in PSS with TNG were calculated for each axis. The results for Group N were as follows: Percentage Systolic Shortening Change in PSS with TNG Mean SD+ Range (PSS) Mean SD+ Range A 48.3 -0.4 3.3 (45 to 55) 2.8 (-5 to +ll) B 38.2 8.7 (30 to ti3) 13.2 6.6 (+6 to +24) C 48.4 16.5 (38 to 81) 10.25 5.6 (-5 to +571 Less than 40, 30, and 3!; PSS was defined as asynergy and increase in PSS of more than 5, 20, and 25 with TNG was defined as supernormal response for A, B, and C Five MI pts had 14 asynergetic axes and respectively. did not change with TNG. There were 24 asynergetic axes in 12 AN pts; 8 showed normal and 16 supernormal response to TNG. In 4 AN pts reversal of asynergy was total and complete with TNG. Thus, the post-nitroglycerin left ventriculography is a simple, safe, and useful test to assess the reversibility of left ventricular asynergy in pts with CAD.
Volume 33