Biomedical subjects
Publications and source records attributed to H Hammerman.
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A case report of a patient with acute myocardial infarction and severe hypoxemia due to acute right to left interatrial shunt (RLIAS) is presented. Diagnostic and therapeutic procedures are discussed.
Long-term follow-up of 5 or more years in 20 patients with initially unresectable cancer of the pancreas that responded to chemoradiation therapy is detailed in this article. All patients underwent resection. Seven or 18 surgical survivors are alive 50 or more months.
BACKGROUND: We have demonstrated previously that, when repeated reperfusion is performed after reocclusion, there is a decrease in the amount of myocardial salvage, despite early reperfusion. Treatment with nisoldipine induced a beneficial effect by reduction of infarct size in this experimental model. OBJECTIVE: To study the effect of HEPES buffer on infarct size, using a repeated-reperfusion model. METHODS: The left anterior descending coronary artery was occluded in anesthetized dogs. Thirty minutes after the occlusion, dogs were allocated randomly to either the treatment group (n = 7; HEPES 0.64 mmol/l infused intravenously throughout the experiment) or the control group (n = 8; saline). Occlusion was maintained for 2 h, followed by 1 h of reperfusion, then 1 h of reocclusion and 2 h of second reperfusion. An in-vivo area at risk was determined by gentian violet staining, and infarct size was defined and quantitated by triphenyl-tetrazolium chloride staining. RESULTS: Hemodynamic measurements were similar in both groups. Mass of necrosis/mass at risk was significantly smaller in the HEPES group (30.7 +/- 1.6%, mean +/- SEM) compared with controls (50.6 +/- 3.8%, P < 0.001). CONCLUSION: Treatment with HEPES induces a beneficial effect by reduction of infarct size in repeated coronary reperfusion.
BACKGROUND: Iatrogenic illness, defined as a disease that results from a diagnostic procedure or from any form of therapy, is a well-recognized phenomenon in clinical practice. OBJECTIVES: To study and evaluate major cardiac iatrogenic disease as the cause of admission to the intensive cardiac care unit in the modern era. METHODS: We assessed 64 critically ill patients suffering from major cardiac iatrogenic problems among a total of 2,559 patients admitted to the intensive cardiac care unit during 3 years. Iatrogenic illness was defined as any problem that resulted from therapy. Only cardiac problems were included in the study. Complications of interventional cardiovascular procedures, suicide attempts or accidental intoxications were excluded. RESULTS: There was evidence of a major cardiac iatrogenic problem as the cause for admission in 64 patients (2.5%): 58 (91%) suffered from arrhythmias (mainly bradyarrhythmias) secondary to beta-blockers, amiodarone, calcium antagonists, electrolyte imbalance or a combination, and 6 (9%) had non-arrhythmic events (hypotension, syncope or acute heart failure). In 41 patients (64%) the iatrogenic event was considered preventable. CONCLUSIONS: Major cardiac iatrogenic complications are an important factor among patients admitted to the intensive cardiac care unit. Most of the events are bradyarrhythmias related to anti-arrhythmic agents. Almost two-thirds of events are preventable.
OBJECTIVES: The aim of this study was to investigate the balance between prooxidative and protective mechanisms in patients with acute myocardial infarction (AMI) throughout streptokinase (STK) therapy. METHODS: Patients who presented to coronary care unit within 3 hours of infarction were followed. Blood was collected before, 2 and 24 hours post STK. Plasma lipid peroxidation was analyzed by a free radical generating system (AAPH) and malondialdehyde equivalents and conjugated dienes quantitated. Plasma vitamins A, E and beta-carotene, were analyzed by HPLC. Patients' results were compared with those from age-matched, healthy control subjects. RESULTS: In 38 patients with AMI, baseline plasma antioxidant vitamin concentration was reduced compared with a healthy control group. Upon STK therapy, there was a significant drop in plasma vitamin E concentration. Successful reperfusion was followed by an increased plasma oxidizability. Plasma lipids were not significantly different in the AMI patients except for a lower HDL-cholesterol concentration. CONCLUSIONS: Patients with AMI showed a drop in plasma antioxidant vitamins. Upon thrombolysis, there was an enhanced lipid peroxidation. These alterations indicate the significance of free radical generation processes in reperfusion injury in AMI patients, and suggest the potential involvement of antioxidants in the management of AMI treated by thrombolysis.
BACKGROUND: We have demonstrated that when repeated reperfusion is performed after reocclusion, there is a decrease in the amount of myocardial salvage, despite early reperfusion. It is unknown whether this deleterious effect of repeated reperfusion can be antagonized. Therefore, we studied the effect of nisoldipine (a dihydropyridine calcium antagonist) on infarct size, using a repeated-reperfusion model. METHODS: The left anterior descending coronary artery was occluded in anaesthetized dogs. Thirty minutes after occlusion, dogs were allocated randomly to either the treatment group (n = 6; 6 micrograms/kg per min nisoldipine infused intravenously throughout the experiment) or the control group (n = 8; saline). Occlusion was maintained for 2 h, followed by 1 h of reperfusion, then 1 h of reocclusion and 2 h of second reperfusion. An in vivo area at risk was determined by gentian-violet staining, and infarct size was defined and quantitated by triphenyl-tetrazolium-chloride staining. RESULTS: Haemodynamic measurements were similar in both groups. Mass of necrosis/mass at risk was significantly smaller in the nisoldipine group (33.3 +/- 5.8%, mean +/- SEM) compared with controls (46.8 +/- 4.8%; P < 0.05). CONCLUSION: Treatment with nisoldipine induces a beneficial effect by reduction of infarct size in repeated coronary reperfusion.
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UNLABELLED: This study aims to test the assumptions that: (1) coronary arterial flow is attenuated in an early activated region by ventricular pacing; (2) asynchronous mechanical activation caused by ventricular pacing under controlled perfusion pressure and intact coronary tone is associated with reduced coronary flow compared to atrial pacing; and (3) abolishment of vascular tone under controlled perfusion pressure diminishes the expected difference in blood flow between atrial and ventricular pacing. Blood flow velocity (BFV) in the left anterior descending (LAD) and the left circumflex arteries (CFX) and a wall thickening index were measured in 14 open-chest dogs under normal conditions, and constant perfusion pressure. Four pacing sites were used: right atrium (RAp), mid-right ventricle (RVp), mid-left ventricle (LVp), and left ventricular apex (Apexp). Pacing modes were either sequential ventriculoatrial (VA) (protocol A, n = 7), or sequential atrioventricular (AV) (protocol B, n = 7), with a shorter AV difference (30 msec) than normal. RESULTS: BFV was decreased in the LAD during RVp and Apexp pacing by 9.7%-12.9% versus RAp and by 11.6%-14.6% versus LVp (P < 0.05). No BFV variations were observed in the CFX. Flow velocity conductance (FVC = mean blood flow velocity divided by the mean aortic pressure) was higher by 16%-28% in the CFX for the three ventricular pacing sites versus the atrial pacing, and higher by 14.1% +/- 6.1% only in LVp versus RAp pacing in the LAD (P < 0.05). Wall thickening index reduced during ventricular pacing in all three ventricular sites by 50%-64% (P < 0.05) compared to atrial pacing. Under constant perfusion pressure, LAD blood flow decreased with ventricular pacing as compared to right atrial pacing; this was particularly pronounced during the diastolic phase (16.6%-45.5%, P < 0.02). Normalized oscillatory flow amplitude (OFAn) was reduced in RVp pacing compared to RAp and LVp pacing (16.2 +/- 3.5 and 21.7% +/- 4.1%, respectively, P < 0.03). The variations in blood flow and OFAn disappeared with adenosine-mediated maximum vasodilatation. SUMMARY: (1) Mean and phasic flows are reduced in the early activated LAD region by ventricular pacing (RVp, Apexp). (2) Under controlled perfusion pressure and intact vascular tone, ventricular pacing compromises blood flow compared with atrial pacing. (3) This effect disappears when vascular tone is eliminated by intracoronary injection of adenosine, suggesting that the coronary autoregulation is responsible for some of the effects.
OBJECTIVE: A preconditioning mimetic agent could be useful therapy for cardiac ischaemic events; stimulation of adenosine receptors has been proposed as a preconditioning mediator. The ability of adenosine-receptor activation to mimic ischaemic preconditioning was tested in an in vivo rabbit model. METHODS: Adenosine (15 mg, a maximally tolerated dose, n = 10) was infused over six minutes via a coronary artery and compared with saline (n = 12) in anaesthetised rabbits. Five minutes after infusion, a coronary artery was occluded for 40 minutes followed by three hours of reperfusion. In a second study, preischaemic intravenous treatment with adenosine (25 mg.kg-1, n = 9), or an A1-adenosine agonist, R(-)-N-(2-phenylisopropyl)-adenosine (PIA, 900 micrograms.kg-1, n = 12), were compared with saline (n = 12), when given before 40 minutes of coronary artery ligation and three hours of reperfusion in anaesthetised rabbits. RESULTS: Intracoronary adenosine reduced mean arterial pressure during infusion (48(3) v 80(4) mm Hg, control, p < 0.001); however, infusion regional myocardial blood flow was significantly higher in adenosine treated hearts (5.00(0.90) v 2.30(0.26) ml.min-1 x g-1, p < 0.02) in the region later to become ischaemic. During occlusion ischaemic blood flow was similar in both groups as was the size of the ischaemic risk region, expressed as a % of the left ventricle (42(3)% adenosine and 37(3)% control, NS). Intracoronary adenosine treatment failed to reduce infarct size (52(5)% of the risk zone v 57(7)% in controls, NS). In the second protocol, heart rate immediately after treatment was reduced by both intravenous denosine (26%) and PIA (22%) v control, indicating atrial A1 receptor activation. Treatment with PIA resulted in a significant reduction in ultimate infarct size compared with saline (38(5)% of risk region v 57(5)%, p < 0.05). Adenosine, however, failed to reduce infarct size (50(8)%, NS v saline). There were no differences between area at risk or myocardial blood flow among groups. CONCLUSION: The adenosine agonist PIA but not adenosine itself might be a useful adjunctive therapy.
Sixty-five patients with symptomatic pancreas divisum were treated by endostents, surgery, or observation. In 35 patients, endoscopic stenting either alone (20) or followed by surgery (15) was the primary therapy. Of 30 patients not stented, 10 underwent elective surgery and 20 were followed. Treatment was based on symptoms and biochemical and radiologic tests. The results of surgical decompression correlated favorably with endoscopic drainage. In untreated patients, the natural history of pancreas divisum was benign. Surgery is safe and effective in symptomatic patients, although multiple operations may be required for recurrent symptoms or progressive disease.
Of 11 patients with gallstone pancreatitis, 10 underwent preoperative ERCP. Calculi were removed from the common duct in two patients. All patients underwent laparoscopic cholecystectomy, with normal rapid convalescence. The eleventh patient is recovering from pancreatitis with the bile duct accessed percutaneously. A combined endoscopic and laparoscopic approach to gallstone pancreatitis is safe and was associated with minimal risk in this small series.
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Pancreas divisum is discussed to define and evaluate criteria for treatment. Selecting candidates for surgery is imprecise since the anatomic anomaly is so prevalent. Endoscopic stenting has been utilized as a therapeutic and diagnostic test. Appraisals of operative results vary depending on length and detail of follow-up. Sphincteroplasty of the dorsal segment is the procedure of choice when the gland is normal--but resection and caudal drainage each have a role, depending on the anatomic and endoscopic findings.
A rigorous mathematical analysis of Electrocardiogram (ECG) data is presented in this paper, as a decision support system for ECG interpretation. The mathematical analysis: provides a new insight to the ECG data, provides flexibility for future understanding of the heart system or the ECG, and avoids the need of measurements of parameters and the disagreement concerning the standard criteria of those parameters. The system enables compressed storage of the ECG data and an easy and accurate retrieval ability. An "ordinal straight line" method is presented for simple description of the ECG features as a combination of straight lines. A new developed discrimination method--the bisector method--is used for discrimination and classification between the normal and pathological groups. The physician's decision is based on both the physician's heuristic approach and the system's classification.
Alterations in afterload may occur during acute myocardial infarction (AMI), but it is unknown whether such alterations cause long-term changes in the left ventricular topography or alter healing of the AMI. AMI was produced by ligation of the left anterior descending coronary artery in open-chest dogs. Eight dogs were randomized to a methoxamine group with an infusion dose of 30 micrograms/kg/min starting 1 hour after ligation for 4 hours to increase systemic systolic pressure by 40 to 50 mm Hg, and 8 were randomized to a saline control group (n = 8). Seven days later the dogs were killed and the hearts examined. The ratio of infarct wall thickness to noninfarct wall thickness was 1.13 +/- 0.03 (mean +/- standard error of the mean) in control dogs and was 0.98 +/- 0.03 in the dogs treated with methoxamine (p less than 0.005). An expansion index was determined as previously reported and expansion was considered to have occurred if this index exceeded 1.09. The expansion index was 0.98 +/- 0.06 in the control group and 1.18 +/- 0.07 in the methoxamine group (p less than 0.05). Histologic analysis suggested a lag in the healing rate in the methoxamine-treated dogs. Thus, early, brief increases in afterload cause infarct expansion and thinning and appears to slow the early healing phase of AMI in dogs.
This study was designed to evaluate whether the effects of coronary reperfusion with or without a pharmacologic agent could be detected in the early hours after infarction by 2-dimensional (2-D) echocardiography applied in a manner analogous to its clinical use. Proximal left anterior descending coronary occlusion was performed in 24 dogs, and the dogs were then randomized into 3 groups. In group 1 (n = 8), coronary occlusion was maintained for 6 hours; in group 2 (n = 8), coronary occlusion was maintained for 2 hours and was followed by 4 hours of reperfusion; in group 3 (n = 8), 2 hours of coronary occlusion were followed by 4 hours of reperfusion but methylprednisolone (30 mg/kg intravenously) was also administered 15 minutes after coronary occlusion. At 6 hours, 2-D images were obtained through the closed chest wall and the percentage of the left ventricular wall motion abnormalities was determined at 4 short-axis levels. The mass at risk was defined by in vivo Monastral blue injection and infarction by triphenyltetrazolium chloride staining. The mass of necrosis was 74 +/- 4% (mean +/- standard error of the mean) of the mass at risk in group 1 and was smaller in groups 2 and 3, 44 +/- 6% and 35 +/- 4%, respectively (p less than 0.01). Percent necrosis of the left ventricle was 22 +/- 3% in group 1, 15 +/- 3% in group 2 (difference not significant) and 10 +/- 2% in group 3 (p less than 0.05 vs group 1).(ABSTRACT TRUNCATED AT 250 WORDS)