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A new artificial aortic valve prosthesis was developed for implantation by the transluminal catheter technique without thoracotomy or extracorporal circulation. The new heart valve was prepared by mounting a porcine aortic valve into an expandable stent. Before implantation, the stent-valve was mounted on a balloon catheter and compressed around the deflated balloon. The stent-valve mounted balloon catheter was then advanced retrogradely to the ascending aorta or the aortic root in anaesthetized pigs. Implantation was performed by balloon inflation which expanded the stent-valve to a diameter exceeding the internal diameter of the vessel--thus ensuring a stable fixation against the vessel wall. A total of nine implantations were performed in seven 70 kg closed chest pigs. Sub- and supracoronary implantation was performed in two and three pigs, respectively, while implantation in both positions was done in two. Angiographic and haemodynamic evaluation after implantation revealed no significant stenosis (less than or equal to 16 mmHg) in any of the nine valves and trivial regurgitation in only two. Complications were associated with restriction of the coronary blood flow in three animals. This preliminary study indicates that artificial aortic valves can be implanted in closed chest animals by transluminal catheter technique.

Incapacitating or life-threatening tachyarrhythmias were treated nonpharmacologically in 249 patients from 1982 to 1991. Among 92 patients surgically treated for supraventricular tachycardia the cure rate was 93% and the complication rate 12%. Radiofrequency catheter ablation gave an equal cure rate in 51 patients, but with no major complications or mortality. Direct-current catheter ablation of the His bundle was successful in 96% of 27 patients with drug-refractory atrial fibrillation or other supraventricular tachyarrhythmias. Among 64 patients undergoing surgery for ventricular tachycardia/ventricular fibrillation, the perioperative mortality was 9%, estimated 5-year survival 69% and estimated 5-year freedom from the preoperative arrhythmias 72%. Of 18 patients treated with implantable cardioverter defibrillator, three (18%) died of heart failure during follow-up. Nonpharmacologic treatment of tachyarrhythmias is concluded to be effective and often definitively curative. The safety-risk ratio is improving as new treatment modalities are developed.

The rate of elimination of mercury after a single oral or intraperitoneal administration of HgCl2 to male or female mice has recently been demonstrated to be inversely related to the dose size (Nielsen and Andersen, 1989, 1990). The present study demonstrates dose-related induction of renal tubular damage, followed by regeneration, after oral administration of HgCl2 to female mice. Dose-related increased fractional urinary mercury excretion (expressed as percent of dose) was also demonstrated. At increasing dose of HgCl2, the renal activity of selenium-dependent glutathione peroxidase decreased, and was only 50% of the activity in untreated controls after administration of 200 mumol HgCl2/kg. At higher doses, the renal concentration of glutathione was significantly reduced as well. The degree of tissue damage was inversely related to the fractional deposition of mercury in the kidneys. This study indicates that the reduction in fractional whole-body retention of mercury with increasing dose size previously demonstrated is due to increased urinary mercury excretion during transient renal damage followed by regeneration, as extensive leakage took place before extensive regeneration was noted.

ST elevation in right chest leads during evolving inferior myocardial infarction indicates right ventricular involvement. Theoretically, such changes may be due to reversible or irreversible myocardial ischemia. Whether similar ST elevations can be recorded in patients with myocardial ischemia without infarction is unknown. To clarify this, right chest leads V3R to V7R were recorded during percutaneous transluminal coronary angioplasty in 43 patients who had a total of 45 arteries dilated. Balloon occlusion of the right coronary artery caused transient ST elevation, whereas closure of the left anterior descending coronary artery or the left circumflex artery was associated with transient ST depression. These findings were 100% discriminative in leads V5R and V6R. Furthermore, ST elevation greater than or equal to 1 mm in one or more of leads V4R to V7R was seen only when the right coronary artery was occluded. Thus transient myocardial ischemia without infarction may cause ST elevation in the right chest leads and ST elevation greater than or equal to 1 mm in one or more leads V4R to V7R is seen exclusively with occlusion of the right coronary artery.

Twelve patients with supraventricular tachycardia refractory to medical management were treated with catheter ablation (fulguration) of the atrioventricular (AV) conduction system followed by pacemaker implantation. All 12 patients had initially 3 degrees AV block. In ten patients it was permanent. One patient had a permanent 1 degree AV block and left bundle branch block. In one patient with initial 3 degrees AV block AV conduction resumed. No major complications were seen. At follow-up, the mean observation period was 15 months (range 3-57 months). All ten patients with permanent 3 degrees AV block were free of arrhythmic symptoms and without any medication. The patient with permanent 1 degree AV block was free of symptoms and arrhythmia, but died 16 months after the ablation. The patient with relapse of the AV conduction continued to have arrhythmic symptoms, but ECG did not confirm arrhythmia. It is concluded that catheter induced 3 degrees AV block is a safe and efficient treatment of patients with supraventricular tachycardia refractory to medical treatment.

The prognostic significance of ST-elevation greater than or equal to 1 mm in right chest leads V3R-V7R during inferior/posterior acute myocardial infarction (AMI) was evaluated in 86 consecutive patients with their first inferior/posterior AMI, and compared with the prognosis for 72 patients with first anterior AMI. At follow-up, the maximum observation time was 3.0 years (mean 1.8 years). A total of 49 patients died. Using Cox multivariate analysis, ST-elevation in right chest leads during inferior/posterior AMI was found to be an independent predictor of the prognosis in patients surviving the initial ten days after infarction (n = 129). For these patients, the cumulative survival was better after inferior/posterior AMI with ST-elevation in V3R-V7R (n = 25) compared with; (1) all other infarcts (n- 104, p = 0.05), (2) inferior/posterior AMI without ST-elevation in these leads (n = 45, p = 0.09), and (3) anterior AMI (n = 59, p = 0.08).

A catheter-transducer system consisting of a thin fluid-filled teflon catheter and a transducer with a low displacement volume is presented. The thin catheter is especially suited for registration of pressure and the time derivatives in small caliber vessels. From theoretical considerations it is concluded that the best way of obtaining a correct damping ratio in the range of 0.6-0.7 in the system is to adjust the diameter of the catheter empirically to the characteristics of the transducer. Residual gas bubbles are a problem in most catheter-transducer systems, but due to the design of the catheter and to a special flushing method, reproducible results are rapidly and easily obtained. The damping ratio of the system is 0.6 and the band width is 35 Hz. In repeated experiments an identical influence of the temperature on the damping ratio could be demonstrated.

ST-segment elevation in right chest leads V3R-V7R and Q wave in V3R was measured early (1-4 hours) and late (18-24 hours) after the onset of infarction in six patients. The patients died within 9 days of infarction, and autopsy demonstrated more than 50% necrosis of the right ventricle (inclusion criterion). Abnormal ST elevation was recorded in all patients in the early and late electrocardiograms, but mean ST elevation decreased significantly between these recordings. ST elevation greater than or equal to 1 mm was recorded in all patients in the early electrocardiogram but was present in only three (50%) in the second electrocardiogram. The number of leads exhibiting abnormal ST elevation decreased from 27 (90%) to 24 (80%) (NS), and those exhibiting ST elevation greater than or equal to 1 mm decreased from 24 (80%) to 15 (50%), (p less than 0.05). Q wave in V3R was present in both electrocardiograms in three patients. Evolution of Q wave was seen in only one patient, whereas two patients were without Q wave in both electrocardiograms. These results indicate that ST elevation in V3R-V7R may vanish within the initial 24 hours despite large right ventricular infarction. Furthermore, Q wave in V3R may evolve very early after the onset of right ventricular infarction.

Earlier reports have indicated, that the platelet sensitivity to prostacyclin (PGI2) is decreased in patients with coronary heart disease and that the onset of a spontaneous anginal attack is associated with a further decrease in platelet sensitivity to PGI2. We studied platelet function before and after bicycle exercise testing in 23 patients with angina pectoris and in 11 healthy males. We could not demonstrate any difference in platelet sensitivity to PGI2 between patients with angina pectoris and the controls neither before or after exercise testing. The platelet sensitivity to PGI2 decreased significantly after exercise, both in patients and in controls, but the decrease was not related to the development of myocardial ischemia. Our results could be interpreted in terms of different pathophysiological roles of platelets in spontaneous and in exercise-induced myocardial ischemia.

The effect of 12 weeks supplementation with fish oil on the number of anginal attacks and consumption of glyceryltrinitrate in 36 patients with stable angina pectoris was evaluated in a clinically controlled trial using a vegetable oil as placebo. Fish oil caused a decrease in frequency of angina, but was not significantly superior to placebo. However, due to the small sample size and a high spontaneous variation in number of anginal attacks, a risk of up to 50% of overlooking a 30% reduction in anginal attacks could be estimated. A significant inhibition of the epinephrine-induced platelet aggregation and a significant increase in intraplatelet cyclic AMP were induced by fish oil.

Non-invasive Dual-Chamber Pacing was performed with low threshold current using a newly developed trans-oesophageal lead-electrode in one healthy volunteer.

The diagnostic accuracy of ST elevation in lead III exceeding that of lead II (ratio III/II greater than 1) in the diagnosis of right ventricular infarction was investigated in 24 autopsied patients with inferior/posterior myocardial infarction on ECG. The results were compared with the diagnostic accuracy of ST elevation greater than or equal to 1 mm in right-chest leads V3R to V7R recorded in the same patients. All had left ventricular infarction documented at autopsy, and 17 (71%) had concomitant right ventricular involvement. The highest specificity (100%) and positive predictive value (100%) were calculated for the right-chest leads, whereas values for ratio III/II greater than 1 were 88% and 91%, respectively. The differences were not statistically significant. It is concluded that differences in ST elevation in leads III and II can be the basis for a diagnosis of right ventricular involvement in ECG-diagnosed inferior/posterior infarction. The diagnosis, however, may be achieved more easily with right-chest leads.

Intraperitoneal administration of cadmium chloride to 8-12 weeks old CBA-mice enhanced hepatic lipid peroxidation. A positive correlation between cadmium chloride dose and level of peroxidation was observed in both male and female mice. A sex-related difference in mortality was not observed but at a dose of 25 mumol CdCl2/kg the level of hepatic lipid peroxidation was higher in male mice than in female mice. The hepatic lipid peroxidation was not increased above the control level in 3 weeks old mice, while 6 weeks old mice responded with increased peroxidation as did 8-12 weeks old mice. The mortality after an acute toxic dose of cadmium chloride was the same in the three age groups. Pretreatment of mice with several low intraperitoneal doses of cadmium chloride alleviated cadmium induced mortality and lipid peroxidation. The results demonstrate both age dependency and a protective effect of metallothionein induction on cadmium chloride induced hepatic lipid peroxidation.

The frequency and size of previous unrecognized myocardial infarction in patients with first clinical diagnosed acute myocardial infarction are unknown. In this study, 53 consecutive patients with clinical first acute myocardial infarction which proved fatal were studied postmortem. All showed acute infarction (inclusion criterium). Acute coronary thrombosis was found in 51 (96%). One-, two-, and three-vessel disease diagnosed by postmortem coronary angiography (diameter stenosis greater than or equal to 75%) was present in 17 (32%), 22 (42%), and 14 (26%), respectively. One or more old infarcts were found in 24 of the cases (45%) despite no history of previous myocardial infarction. Old infarcts were found in 86% of the hearts with three-vessel disease and in 55% of the hearts with two-vessel disease, but none were found in the hearts with one-vessel disease. The median weight of the old infarcts was 4 grams (range: 0.5 to 25 grams) corresponding to 5% (0.5 to 14%) of the ventricular myocardium. Thus, two- or three-vessel coronary artery disease and old infarcts are often present in patients dying from their clinical first acute myocardial infarction.

Intraperitoneal administration of nickel chloride enhanced hepatic lipid peroxidation (HLP) in 6-wk-old and 8-12-wk-old male CBA-mice but not in 3-wk-old mice. Nickel chloride administration depleted hepatic GSH in 8-12-wk-old mice but not in the younger age groups. After 300 mumol NiCl2/kg mortality occurred among 8-12-wk-old mice but not among the younger mice. Stimulation of GSH synthesis by administration of L-2-oxothiazolidine-4-carboxylate reduced nickel chloride induced mortality and HLP. Reduction of GSH synthesis by administration of buthionine sulfoximine (BSO) did not, however, enhance the toxicity of nickel chloride. This might be owing to chelation of the Ni(II)-ion by BSO. The results demonstrate age dependency and a protective effect of enhanced GSH synthesis in nickel chloride stimulated HLP.

During a 14 month period autopsies were performed on 107 patients with coronary heart disease and the results were evaluated prospectively with special reference to right ventricular infarction. A total of 214 regional infarcts were found, 107 (50%) of which involved the right ventricle. Right ventricular infarction was found in 90 hearts (84%), but only three isolated right ventricular infarcts were seen. Right ventricular involvement was found with equal frequency in anterior and posterior infarction (64 versus 66%), but posterior right ventricular infarcts were much larger (15% of the right ventricle was infarcted versus 1%). Proximal right coronary artery occlusion caused larger right ventricular infarction than did distal occlusion (15 versus 5 g). Right ventricular infarct size was not influenced by coronary artery disease (evaluated angiographically) in noninfarct-related vessels. Anterior right ventricular infarcts were predominantly located near the apex of the heart (to the left of the sternum), whereas posterior right ventricular infarcts were located near the atrioventricular groove (along the right sternal border). Infarct size was equal in patients who died from a first acute anterior or posterior infarct. However, posterior infarcts had more right ventricular involvement (28% of total infarct size versus 7% in anterior infarcts) leaving more of the left ventricular myocardium intact (79 versus 64%). These differences in infarct topography may explain why right ventricular involvement seldom is diagnosed clinically in patients with anterior infarction, and why left ventricular function and prognosis usually are better after posterior compared with anterior infarcts of enzymatically equal size.

A 78-year-old man with atherosclerotic heart disease developed extensive right ventricular infarction fibrosis with aneurysm formation following right coronary artery occlusion. No symptoms of right-sided heart failure were present. Postmortem examination revealed that 40% of the right ventricle, 11% of the septum and 7% of the left ventricular free wall were infarcted due to right coronary artery occlusion. This is the first documented case of isolated aneurysm of the right ventricle following infarction and it demonstrates that even extensive right ventricular destruction may be present without symptoms.

Right chest leads, V3R-V7R were recorded in 109 persons (40 women, 69 men, mean age 41 years) without evidence of heart disease. An rS or rSr' configuration was found in V3R in 98% and in V4R in 91%. Secondary r waves increased in amplitude and frequency in lateral leads and were found in V7R in 65%. The r or r' waves did not exceed 5 mm in amplitude in any lead. A qS configuration was found most frequently in V6R (16%) but none had qS configuration in all leads. An r/s ratio greater than one was found in eight persons, but the ratio never exceeded 1.5. Measurements of r and S wave amplitudes and ST-segment deviations in V4R in a 45 degree sitting position including deep inspiration and expiration did not change the amplitudes significantly. Normal values for QRS-amplitudes and q-duration, J-point and ST-segment measured 40 msec and 80 msec after the last QRS-deflection are presented.

Ventricular tachycardia and fibrillation can be converted to sinus rhythm by DC-countershock. An implantable cardioverter defribillator (ICD) has been developed. The apparatus monitors the heart rhythm continuously, detects ventricular tachycardia and ventricular fibrillation and delivers one or more DC-counter shocks a few seconds after the dysrhythm has started. This always ensures rapid treatment, even if the patients is outside hospital. Two case histories are presented and the ICD treatment is discussed.

A new lead-electrode for trans-esophageal pacing of the human heart has been developed. The heart can be paced from the esophagus using currents of the same intensity as those for temporary pacing electrodes. The lead allows the electrodes to be positioned properly in the esophagus with a gastric balloon without use of additional equipment. Noninvasive atrial or ventricular pacing can thus be established quickly, even by non-specialized physicians. The method has been tested on a group of 13 healthy volunteers. Both atrial and ventricular pacing were performed without discomfort. The method opens new diagnostic and therapeutic possibilities with trans-esophageal pacing techniques.

To evaluate whether the right ventricle releases significant amount of cardiac enzymes during myocardial infarction, a clinicopathologic study of 50 patients with 60 infarcts was performed. Myocardial infarct size was determined at autopsy and compared with the corresponding peak serum lactate dehydrogenase and aspartate aminotransferase. Anterior and posterior infarcts had similar anatomic size, peak enzyme values, and coefficients of correlation (r = 0.86-0.88 versus r = 0.82-0.84 for lactate dehydrogenase). However, by disregarding the right ventricular infarct component considering the left ventricular infarction only, the coefficient of correlation between infarct size and peak serum lactate dehydrogenase decreased from r = 0.84 to r = 0.59 (P = 0.09), in 14 posterior infarcts while no change was observed in 24 anterior infarcts (r = 0.88). This indicates, that a considerable amount of enzymes released during posterior infarction originated from the right ventricle which was not the case for anterior infarction.

The accuracy of ST elevation greater than or equal to 1 mm in right chest leads V3R to V7R in the diagnosis of right ventricular infarction was investigated in a clinical and necropsy study of 43 consecutive patients who died in a coronary care unit. Thirty six patients had left ventricular myocardial infarction and in 27 the right ventricle was also affected. Seven patients had normal hearts. The specificity and positive predictive value of ST elevation in V3R were 81% and 77%, respectively. These increased to 100% when combined with ST elevation in one or more leads V4R-V7R. The diagnostic accuracy was poor for anterior infarcts (sensitivity less than or equal to 27%), but high for inferior/posterior infarcts (sensitivity greater than or equal to 64%) in which the specificity and positive predictive value reached 100% in V6R and V7R. Inferior/posterior infarction affecting the right ventricle can be diagnosed reliably by examination of electrocardiograms from right chest leads V6R and V7R.

The prognostic significance of electrocardiographic "extensive right ventricular infarction" diagnosed by ST elevation greater than or equal to 1 mm in right chest leads V3R to V7R during inferior/posterior infarction was evaluated in 158 consecutive patients with first anterior (n = 72) or inferior/posterior (n = 86) myocardial infarction. At follow-up the maximum observation time was 3.0 years (mean 1.8 years). A total of 49 patients died; 96% due to cardiac causes. Twelve patients (8%) died during the first 24 hours of admission. Ten-day mortality was 18% (n = 29). Using Cox multivariate analysis ST elevation in right chest leads during inferior/posterior infarction was an independent predictor of prognosis in patients surviving the initial 10 days after infarction (n = 129). For these patients the cumulative survival was better after inferior/posterior infarction with ST elevation in V3R to V7R (n = 25) compared with (1) inferior/posterior infarction without St elevation in these leads (n = 45, P = 0.09), (2) anterior infarction (n = 59, P = 0.08), and (3) all other infarctions (n = 104, P = 0.05). Infarct size estimated by the peak serum enzyme values was similar in these groups. Thus, electrocardiographic extensive right ventricular infarction predicts a good prognosis in patients alive 10 days after infarction. Compared with infarcts of similar size but with another location the prognosis is better, probably due to concomitant smaller left ventricular infarction with better left ventricular function following infarction.