Biomedical subjects

D J Wu

Publications and source records attributed to D J Wu.

At least 37 records · Page 2Linked to original sources

PubMed1991

Potential diagnosis of hemodynamic abnormalities in patent ductus arteriosus by cine magnetic resonance imaging.

Cine magnetic resonance imaging was performed in 11 patients with communication between systemic and pulmonary circulation. In five patients with uncomplicated patent ductus arteriosus (PDA), ductus arteriosus was delineated by a persistent band of low signal intensity, whereas in two patients who also had severe pulmonary hypertension the signal intensity was varied. Two separate low signal intensities in the main pulmonary artery and the descending aorta were each uniformly recorded in the five patients with uncomplicated PDA, consistent with continuous left-to-right shunt and turbulent flow acceleration, respectively. In one of the patients with severe pulmonary hypertension but not Eisenmenger's syndrome, the areas of low signal intensity from left-to-right shunt and turbulent flow acceleration diminished. In the patient with Eisenmenger's PDA the right-to-left shunt was also characterized by an area of low signal intensity but with a reversal in direction. Cine MR imaging has the potential to be a noninvasive and supplemental method for evaluating PDA.

Adolescent↗

PubMed1991

Intracranial calcification and brachydactyly mimicking Albright's hereditary osteodystrophy in an adult patient with lingual thyroid and prolactinoma-like lesion.

Hyperprolactinemia and prolactinoma in patients with long-term primary hypothyroidism have been recognized for decades. We report a case of 57-year-old female patient with lingual thyroid and cretinism who had a high serum prolactin level (greater than 200 ng/ml) and a pituitary tumor with suprasellar and parasellar extension. The tumor regressed to a size undetectable by CT scan after 2 years of thyroid hormone replacement therapy, but complete normalization of the hyperprolactinemia required additional bromocriptine therapy. This patient showed generalized short metacarpal and phalangeal bones, calcification of the basal ganglia and dentate nuclei bilaterally, and subcutaneous calcification at both gluteal regions, while serum calcium, phosphorus and c-PTH levels were all normal. Thus in addition to short stature, brachydactyly, a round face, and obesity, which are related to hypothyroidism, she also presented features uniquely mimicking the Albright's hereditary osteodystrophy seen in patients with pseudohypoparathyroidism and pseudopseudohypoparathyroidism. Since she had no family history of pseudohypoparathyroidism and had a normal level of Gs alpha protein on the membrane of the red blood cells, there is no evidence of pseudopseudohypoparathyroidism. The cause of the ectopic calcification remains unknown.

Brain Diseases↗

PubMed1990

Clinicopathological study of myocardial infarction with normal or nearly normal extracardiac coronary arteries. Quantitative analysis of contraction band necrosis, coagulation necrosis, hemorrhage, and infarct size.

In order to clarify the pathogenesis of acute myocardial infarction (MI) in hearts with normal coronary arteries, infarct size, and the extent of contraction band necrosis (CBN), coagulation necrosis, and hemorrhage were quantitatively examined using an image analyzer in 5 autopsy cases of MI with normal or nearly normal extracardiac coronary arteries. One patient died 40 h after acute MI. A second patient with acute MI due to severe spasm of segment 6, confirmed by cineangiography, died three days later. The third patient had already suffered a subarachnoid hemorrhage, and died 10 h after the onset of acute MI. The fourth patient had aortic stenosis and regurgitation. She developed acute MI due to total occlusion of segment 6, confirmed by cineangiography 4 h after the onset, and died 61 days later. Autopsy revealed old anteroseptal MI with normal coronary arteries and valvular thrombi. The fifth patient had a malignancy, and died one day after the onset of acute MI. Autopsy revealed multiple occlusive thrombi in the small intramural coronary arteries of the left ventricular wall supplied by segment 14, without any stenosis in the feeding vessel. Most infarcts were localized in the territory supplied by 1 or 2 of the 3 epicardial coronary arteries, and coincided with the clinically diagnosed infarct site. The infarct size ranged from 3%-26% of the left ventricular wall, and infarcts were generally localized to the inner third of the wall (67 +/- 20%). Histological examination of the four patients with acute MI revealed diffuse CBN (86 +/- 14% of the infarcted area) and/or hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

Anginal attack following a sodium bicarbonate and hydrocortisone injection.

A case of a 73-year-old man with variant angina who developed chest pain and shock following an injection of sodium bicarbonate and hydrocortisone is reported. The electrocardiogram (ECG) during the chest pain attack revealed ST elevation in leads II, III and aVF. It returned to a normal pattern 10 min later. Coronary angiography, performed 2 hours after the anginal attack, showed no significant coronary arterial stenosis. One month later, an injection of ergonovine (16 micrograms) into the right and left coronary arteries induced spasms in segments 4 and 13, with ischemic ECG changes. Possible causes of the anginal attack are a coronary arterial spasm induced by the allergic reaction to hydrocortisone and/or serum alkalosis due to the sodium bicarbonate injection triggered by hyperventilation.

Aged↗

PubMed1989

Acceleration of cell necrosis following reperfusion after ischemia in the pig heart without collateral circulation.

A study of whether reperfusion accelerates cell death was performed in 35 pig hearts without collateral circulation. In 15 animals, the distal one-third of the left anterior descending coronary artery was occluded for 1 hour followed by 1-, 3-, or 7-hour reperfusion in 5 animals each. As controls, 5 hearts each were examined after 1, 2, 4 and 8 hours of occlusion of the artery without reperfusion. Heart rate and aortic pressure before and during occlusion and reperfusion did not change in any group. The subepicardial and subendocardial regional blood flow decreased to almost zero in all hearts after occlusion (85 +/- 1 to 2 +/- 2) but recovered during reperfusion (65 +/- 15 ml/100 g/min). Specimens were histologically examined by an enzyme method using nitrotetrazolium blue, an immunohistochemical method using myoglobin antibody, by staining with hematoxylin-eosin and Masson's trichrome. In the control hearts, clear demarcation of the infarct area was observed 4 hours after occlusion. However, in the reperfusion group, clear demarcation of the infarct was seen after 1-hour reperfusion, namely, 2 hours after the onset of infarct. Demarcation was seen not only in the tissue with contraction band necrosis, but also in the tissue with coagulation necrosis. Therefore, it is concluded that reperfusion accelerates cell death due to both contraction band necrosis and coagulation necrosis.

Animals↗

PubMed1989

Response of large and small coronary arteries of pigs to intracoronary injection of acetylcholine: angiographic and histologic analysis.

With coronary arteriography we examined the effect of acetylcholine (ACh) on large and small coronary arteries. ACh (12.5 to 200 micrograms) was injected into the right coronary arteries of 10 pigs during left ventricular pacing. The percentage of narrowing of the epicardial major coronary artery was used as an indicator of the constriction of the large coronary arteries, and the time required for the contrast medium to reach the posterior descending coronary artery from the ostium of the right coronary artery (blood-flow delay) was used as an indicator of the constriction of the same coronary arteries. A small dose of ACh (12.5 to 100 micrograms) induced mild narrowing (14 to 41%) of the epicardial major coronary artery and a marked blood-flow delay of over 7.0 sec (control: less than or equal to 1.8 sec) in all 10 pigs. A large dose of ACh (100 to 200 micrograms) caused over 75% narrowing of the epicardial major coronary artery and a marked blood-flow delay in 4 of the 10 pigs. When the marked blood-flow delay appeared, the perfused right ventricular myocardium became macroscopically anemic (ischemic). The constriction of large and small coronary arteries was not prevented by diphenhydramine (H1 blocker: 100 mg i.v.), but was prevented by pretreatment with atropine (1.0 mg i.v.). The intracoronary injection of histamine (1.5 mg) in 5 pigs constricted the epicardial major coronary artery over 75% in 2 pigs, 50 to 75% in 1 pig, and 25 to 50% in 2 pigs, but there was no evidence of blood-flow delay. Neither methoxamine nor norepinephrine caused any significant coronary artery narrowing. The histology of the large and small coronary arteries was examined quantitatively with an image analyzer. The coronary artery showed no intimal thickening, and the endothelium was intact on light microscopic examination. The % area of the smooth muscle layer (media) to the calculated total vascular area, and the ratio of the calculated medial thickness to the calculated inner radius (h/Ri) were 64 +/- 7% (mean +/- SD) and 0.69 +/- 0.16, respectively, in the small coronary arteries less than 100 microns in external diameter, 47 +/- 9% and 0.39 +/- 0.12 in the small coronary arteries 100 to 2000 microns in external diameter, and 34 +/- 4% and 0.24 +/- 0.03 in the large right coronary arteries over 2000 microns in external diameter; the % area of the media and the h/Ri showed a negative correlation with the size of the coronary arteries.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗

PubMed1989

Influence of propranolol on high energy phosphate and tissue acidosis in regional ischemic myocardium of pigs: assessment with arterial pressure and respiration gated in vivo 31-phosphorus magnetic resonance spectroscopy.

In an attempt to define the metabolic abnormalities of the ischemic myocardium, the changes in high energy phosphates, inorganic phosphate and intracellular pH were serially and quantitatively evaluated in ischemic porcine hearts having no collateral circulation, using arterial pressure and respiration gated in vivo 31P magnetic resonance spectroscopy. The protocol was also modified for propranolol pretreatment (0.6 mg/kg intravenously) to define its effect on the metabolism of ischemic myocardium. In the non-treated group, creatine phosphate was rapidly depleted by 10 minutes after ischemia; by 40 minutes, ATP and intracellular pH gradually decreased to 10 +/- 11% of control and to 5.90 +/- 0.26, respectively, and inorganic phosphate rose to 303 +/- 43% of control. In the propranolol treated group, the concentrations of creatine phosphate and ATP were higher, and those of inorganic phosphate and tissue pH were similar compared with controls during 40 minutes of ischemia. This suggests that the beneficial effect of propranolol on the ischemic myocardium is due to the preservation of ATP, an essential energy resource for numerous enzymatic reactions in viable myocardium.

Acid-Base Equilibrium↗

PubMed1989

Cineangiographic and pathological features of the infarct related vessel in successful and unsuccessful thrombolysis.

The postmortem histology and the results of cineangiography after selective intracoronary thrombolysis in vessels that were recanalized and in those that were not were compared in 21 patients who died within seven days (mean 2 days) of selective intracoronary thrombolysis. There was a persistent intraluminal thrombus in the infarct related coronary artery in five of six segments in which recanalisation was unsuccessful and in one of 15 segments in which recanalisation was successful. Rupture and haemorrhage of the atheromatous plaque were seen in most of the infarct related segments, both in those in which recanalisation was achieved and in those in which it was not. Irregular narrowing and filling defects on the coronary cineangiograms were associated with rupture and haemorrhage of the atheromatous plaque. These results suggest that failure of coronary thrombolysis to recanalize the infarct related artery does not indicate that the occlusion was not caused by thrombus.

Aged↗

PubMed1989

Deficient erythrocyte membrane Gs alpha activity and resistance to trophic hormones of multiple endocrine organs in two cases of pseudohypoparathyroidism.

Patients with pseudohypoparathyroidism (PHPT) have been shown to have deficient cell membrane stimulatory GTP-binding regulatory protein activity (Gs activity) and other defects, which cause renal resistance to parathyroid hormone (PTH). Those patients also have a higher incidence of deficiency of other endocrine axes. To investigate the mechanisms of this syndrome on 2 patients, we measured erythrocytic ghost Gs activity by ADP-ribosylation method, which showed low and low normal levels for the 2 patients who were from the same family, suggesting type Ia of this syndrome. While basal T3, T4 and TSH were compatible with mild primary hypothyroidism in both patients, a TRH test showed exaggerated TSH responses. The estrogen, progesterone and testosterone levels were low and LH and FSH responses were marginally high, indicating gonadal resistance to gonadotropins. ACTH levels were also elevated and ACTH response to CRH was exaggerated in one patient, suggesting additional primary adrenal insufficiency. This finding indicates that systemic endocrine tests are essential for the management of PHPT patients who may have a deficiency of multiple endocrine axes subclinically.

Adolescent↗

PubMed1989

High frequency of spontaneous acute myocardial infarction due to small coronary artery disease in dead (NZWxBXSB)F1 male mice.

To determine whether or not male (NZWXBXSB)F1 [WXB)F1) mice exhibiting a lupus-like syndrome died of acute myocardial infarction (MI), and whether acute MI is directly related to small coronary artery disease, acute and old MIs were examined histologically in 55 dead (WXB)F1 male mice and 30 age-matched, surviving (WXB)F1 male mice used as a control group. In each heart from the 15 dead mice with MI and the five surviving mice without MI, 300 to 400 5-microns-thick serial sections were made; every fourth section was stained. Acute MI was found in 35 (64%) dead mice and in one (3%) survivors, whereas old MI was found in 50 (91%) dead mice and 17 (57%) survivors: a significant difference between the dead and surviving mice. The MIs were numerous, scattered, and small in most mice. Quantitative analysis revealed that the percentage of acute MI and old MI in the left ventricular (LV) wall was 6% +/- 11% and 3% +/- 3% in the dead group, and 0.4% and 2% +/- 3% in the control group. This indicated that recurrent acute MI is a major factor in the death of the mice. Although all the epicardial major coronary arteries of the (WXB)F1 male mice were intact, significant stenoses were noted in the intramyocardial small arteries. The serial sections in the 15 dead mice with MI revealed 1) segmental occlusive thrombi in the infarct-related small coronary artery in 14 of the 20 foci of acute anemic MIs, two of the 18 foci of acute hemorrhagic MIs, and four of the 58 foci of old MIs; and 2) segmental intimal thickenings in the infarct-related small artery in six of the 20 foci of acute anemic MIs, two of the 18 foci of acute hemorrhagic MIs, and 56 of the 58 foci of old MIs. There was no evidence of small coronary artery disease in the surviving mice without MI. The thrombus would result in thickened intima as MI progresses from the acute to the old stage. Because it was established that acute MI of hemorrhagic type follows reperfusion after transient occlusion of the coronary artery, hemorrhagic acute MI with rare incidence of thrombi in this mouse suggests that thrombolysis occurs after occlusion due to thrombus formation. Thus, the pathogenesis of multiple MIs is occlusive thrombi, recanalization in small coronary arteries or both. Some of the mice had dilated cardiomyopathy (DCM)-like features (marked LV dilatation).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1989

[Correlations between results of selective intracoronary thrombolysis and histologic findings of the infarct-related coronary arteries].

To define the histopathogenesis of successful and unsuccessful recanalization following selective intracoronary thrombolysis, coronary angiography (CAG) in thrombolysis and histologic findings were compared in 13 patients who died within four days (mean 1.5 days) after the procedure. Thirteen infarct-related arteries were evaluated in respect to recanalization; presence of an intraluminal thrombus, and rupture and hemorrhage of atheromatous plaques were histologically evaluated in serial sections. Intraluminal thrombi of the infarct-related coronary artery were found in all of the five cases with unsuccessful recanalization and in none of the eight cases with successful recanalization. Rupture and hemorrhage of atheromatous plaques in infarct-related arteries were observed in all of the five cases with unsuccessful recanalization and in seven of the eight cases with successful recanalization. It was concluded that 1) in recanalized cases, thrombi are considered to be lysed; 2) unsuccessful recanalization does not necessarily indicate the absence of thrombi; and 3) rupture and hemorrhage of atheromatous plaques do not affect recanalization.

Aged↗

PubMed1988

Distribution and progression of coronary arterial and aortic lesions in the conventional Watanabe heritable hyperlipidemic rabbit--quantitative analysis.

The distribution and progression of coronary arterial and aortic lesions were examined in 40 conventional Watanabe heritable hyperlipidemic (WHHL) rabbits. They were classified according to age into stage I (3-5 months old, 14 rabbits), stage II (6-12 months old; 12 rabbits) and stage III (14-28 months old; 14 rabbits). Fifteen normal Japanese rabbits served as controls. The findings obtained from serial and transverse sections of each of the extramural coronary arteries (ECA) and transverse sections of 4 to 5 equal pieces of whole ventricle for intramural coronary arteries (ICA) were quantified by an image analyzer. Atherosclerosis with positive Sudan III stain was seen in aorta, ECA and ICA over 200 mu in diameter. Atherosclerotic lesions were noted in the aortic arch in stage I rabbits and in the whole aorta in stages II and III rabbits. In ECA, stenosis due to atherosclerosis was noted in 14, 33 and 93% of stages I, II and III rabbits, respectively. Stenosis of over 75% in the orifices of the left and right coronary arteries was noted frequently (71%), while mural thrombi, hemorrhage, intimal rupture and recanalization were seen rarely. Striking features were non-atherosclerotic stenosis with negative Sudan III, seen in the ICA less than 200 mu in diameter of almost all the hearts of stages II and III rabbits. Acute and old myocardial infarction appeared in 5 of the 14 hearts of the stage III rabbits and the infarct-related ECA showed severe stenosis of over 90%. In conclusion, to detect coronary atherosclerosis, serial and transverse sections of ECA are needed. In conventional WHHL rabbits, the incidence of stenosis in ECA is very high, compared with that of the previous reports, and myocardial infarction is due to severe stenosis in ECA. Non-atherosclerotic lesions in ICA occur before the appearance of the atherosclerotic lesions in ECA.

Animals↗

PubMed1988

Detection of early myocardial infarction in formalin-fixed, paraffin-embedded tissue.

Whether the early infarct area in formalin-fixed, paraffin-embedded tissue could be delineated by the immunohistochemical method using myoglobin-antibody was studied in 23 pig hearts without collateral circulation. Five hearts were examined at 20 minutes, 2 hours, 4 hours, and 6 hours after occlusion of the distal one third of the left anterior descending coronary artery, respectively. Three pigs were killed 24 hours after occlusion. Heart rate and aortic pressure before and after occlusion did not change in any groups. The subepicardial and subendocardial regional blood flows were reduced to almost zero in all hearts after occlusion (0.88 +/- 0.10 to 0.02 +/- 0.02 mL/g/min). Slight myoglobin defects in the ischemic tissue were noted in the five pigs examined 2 hours after occlusion and definite myoglobin defects were detected in all pigs examined at 4, 6, and 24 hours after occlusion. Nitrotetrazorium blue stain of myocardial tissue before formalin fixation showed slight demarcation of the ischemic area at 4 hours after occlusion and definite demarcation at 6 and 24 hours after occlusion. Slight demarcation was noted at 2 hours after occlusion in Masson trichrome stain and 4 hours after occlusion in the hematoxylin-eosin stain. However, definite demarcation of the ischemic area was seen in Masson trichrome stain only at 24 hours after occlusion and was not noted in hematoxylin-eosin stain even at 24 hours after occlusion. Our previous electron microscopic study revealed that, in the pig heart, irreversible cellular damage was transmurally seen at two hours after occlusion of the coronary artery. Therefore, a definite myoglobin defect reflects irreversible cellular damage such as infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Quantitative analysis of contraction band and coagulation necrosis after ischemia and reperfusion in the porcine heart.

To assess the importance of contraction band necrosis (CBN) in reperfusion, CBN, coagulation necrosis (CN), and infarct size, expressed as CBN + CN, were quantitatively analyzed in 25 porcine hearts without collateral circulation. The left anterior descending coronary artery was ligated for 20, 30, 60, and 120 min and then reperfused for 8 hr (groups 1 to 4, respectively). Five hearts were not reperfused (group 5). The areas of CBN and CN were traced at a magnification of X 100 under an inverted microscope and quantified with use of an image analyzer. There was no change in hemodynamics with either occlusion or reperfusion. Regional myocardial blood flow, measured by the generated hydrogen gas clearance method, decreased to almost zero after occlusion but recovered during reperfusion. Percent of risk area infarcted in groups 1 to 4 was 0 +/- 0%, 11 +/- 7%, 80 +/- 9%, and 96 +/- 2%, respectively, and the percent of risk area infarcted in group 4 was the same as that in hearts subjected to permanent occlusion (95 +/- 3%). The percent area of CBN was 100 +/- 0% in group 2, 68 +/- 11% in group 3, 2 +/- 1% in group 4, and 2 +/- 2% in group 5. In group 3, the inner third of the ischemic left ventricular wall showed CN and the middle and outer third CBN. These findings show that in pig hearts without collateral circulation, the transmural infarct, two-thirds of which is occupied by CBN, is evident even when reperfusion is achieved after 1 hr occlusion. Therefore, protection against CBN might reduce infarct size after reperfusion.

Animals↗

PubMed1987

Quantitative analysis of narrowings of intramyocardial small arteries in normal hearts, hypertensive hearts, and hearts with hypertrophic cardiomyopathy.

To clarify the pathophysiologic role of intramyocardial small artery (IMSA) diseases in hypertrophied hearts, narrowings of the IMSA were quantitatively evaluated in 39 autopsied hearts, 10 from patients with typical hypertrophic cardiomyopathy (HCM), four from patients with HCM showing features mimicking dilated cardiomyopathy (DCM-like HCM), 10 from patients with hypertension, and 15 from normal adults. The relations of narrowings of the IMSA to myocytic hypertrophy, myocardial fiber disarray, and fibrosis were also examined. The external caliber and the ratio of the luminal area to the total vascular area (percent luminal area, % lumen) were calculated by an image analyzer in 85 to 203 IMSAs from each patient. The external calibers of the IMSAs were similar among groups of hearts with HCM, hypertensive hearts, and normal hearts but were greater in those with DCM-like HCM. The mean % lumen of the IMSAs was similarly reduced in the hearts with HCM (29 +/- 5% in the ventricular septum and 31 +/- 5% in the left ventricular free wall) and in hypertensive hearts (30 +/- 8% and 31 +/- 7%) compared with that in normal hearts (40 +/- 5% and 38 +/- 5%) and was the lowest in the ventricular septum of hearts with DCM-like HCM (17 +/- 3%). The mean % lumen of the IMSA was inversely correlated with heart weight (r = -.59), the mean size of myocytes (r = -.66 in the ventricular septum, r = -.63 in the free wall), and percent fibrotic area in the septum (r = -.68). The mean % lumen values of the IMSAs in the tissues with and without disarray in the hearts with HCM were similar. Thus IMSA disease is of pathophysiologic importance in patients with HCM, DCM-like HCM in particular, or with hypertension.

Adult↗

PubMed1987

Quantitative analysis of infarct size, contraction band necrosis, and coagulation necrosis in human autopsied hearts with acute myocardial infarction after treatment with selective intracoronary thrombolysis.

To assess the importance of contraction band necrosis (CBN) in patients with acute myocardial infarction (AMI) treated with selective intracoronary thrombolysis, CBN, coagulation necrosis, and infarct size (expressed as CBN + coagulation necrosis) were analyzed quantitatively in 16 autopsied hearts. Intracoronary thrombolysis was performed from 2 to 6 hr after the onset of AMI, and the time from the onset of AMI to death was 7 to 168 hr. Cineangiography revealed no evidence of good collateral circulation in any of the patients. The 16 patients were classified into three groups: six patients with successful thrombolysis (100% to 99% stenosis, group I), five patients with unsuccessful thrombolysis (100% to 100%, group II), and five patients with 99% stenosis before thrombolysis (group III). Among the three groups, there were no significant differences in the time from the onset of AMI to thrombolysis, the time from the onset of AMI to death, the cause of death, or the degree of collateral circulation. The percentage of the risk area involved by the infarct in group I (82 +/- 6%) was similar to that in group II (80 +/- 11%). Infarct size was not reduced in group I because collateral circulation was not good and because the degree of recanalization after thrombolysis was 1%. However, the percentage of the infarct area with CBN was significantly higher in group I (20 +/- 9%) then in group II (3 +/- 3%). This finding shows that diffuse CBN occurred after reperfusion in patients with AMI treated with thrombolysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1987

Limitation of coronary thrombolysis: experimental study of reperfusion after ischemia.

Contraction band necrosis (CBN), coagulation necrosis (CN) and infarct size, expressed as CBN + CN, were quantitatively analyzed in 15 pig hearts without collateral circulation. The left anterior descending coronary artery was ligated for 60 and 120 minutes and then reperfused for eight hours (group 1 and 2, respectively). Five hearts were not reperfused (group 3). There was no change in hemodynamics with either occlusion or reperfusion. Regional myocardial blood flow, measured by the generated hydrogen gas clearance method, decreased to almost zero after occlusion but recovered during reperfusion. Percent infarct area of the perfused area in group 1, 2 and 3 were 80 +/- 9, 96 +/- 2% and 95 +/- 3%, respectively. The percent area of CBN was 68 +/- 11% in group 1, 2 +/- 1% in group 2 and 2 +/- 2% in group 3. We conclude that in pig hearts without collateral circulation, the transmural infarct, two-thirds of which is occupied by CBN, is evident even in reperfusion following one-hour occlusion. Therefore, in patients with acute myocardial infarction, coronary thrombolysis should be performed within one hour after the onset of the infarction to reduce the infarct size.

Animals↗

PubMed1987

Pathogenetic role of myocardial fiber disarray in the progression of cardiac fibrosis in normal hearts, hypertensive hearts and hearts with hypertrophic cardiomyopathy.

To define the pathogenetic role of myocardial fiber disarray in the progression of cardiac fibrosis, the percent area of fibrosis in tissue with disarray was compared with that in tissue without disarray. Thirty autopsied hearts, 10 from patients with hypertrophic cardiomyopathy, 10 from patients with hypertension and 10 from normal adults, were studied. The percent areas of fibrosis in tissues with and without disarray were significantly different (p less than 0.01) among hearts with hypertrophic cardiomyopathy (12.6 +/- 4.0 and 8.2 +/- 3.3%), hypertensive hearts (6.6 +/- 3.6 and 2.5 +/- 1.4%) and normal hearts (2.8 +/- 1.2 and 1.0 +/- 0.4%). The percent area of fibrosis in tissue with disarray was greater than in that without disarray in all 3 groups and the ratios of these percentages were similar in the 3 groups: 2.9 +/- 4.2 in hypertrophic cardiomyopathy 2.5 +/- 1.7 in hypertensive hearts and 2.5 +/- 1.8 in normal hearts. The conclusions are: 1) disarray promotes fibrosis to a similar degree, not only in hypertrophic cardiomyopathy, but also in hypertensive hearts and normal hearts; 2) the increased level of fibrosis in hearts with hypertrophic cardiomyopathy and in hypertensive hearts, together with widespread fibrosis in hearts with hypertrophic cardiomyopathy in particular cannot be explained by disarray alone.

Cardiomegaly↗