Prognosis after myocardial infarction: results of 15 year follow up.

A total of 271 out of 757 patients who had suffered a myocardial infarction during 1966-7 were still alive after six years; these patients were subsequently followed up 15 years after the infarction. Two hundred and sixty eight (99%) of the patients alive at six years and 519 (95%) of the 549 originally discharged from hospital were traced. A coronary prognostic index, which had predicted survival both to three years and from three to six years after recovery from the infarct also predicted survival from six to 15 years after recovery. The major factor affecting survival to 15 years was age at the time of the original infarct. Among patients aged under 60 at the time of infarction women fared better than men (p = 0.027). Factors in the coronary prognostic index that were associated with impairment of left ventricular function at the time of infarction and that had predicted mortality to three years and from three to six years also predicted mortality from six to 15 years. These factors were cardiac enlargement, pulmonary venous congestion, and the presence of infarction before the index infarct. The dominant cause of death remained coronary heart disease and its complications.     

Oxygen Transport in Acute Pulmonary Oedema and in Acute Exacerbations of Chronic Bronchitis

When breathing air, the average arterial oxygen tension in eight patients with acute pulmonary oedema was significantly higher than in eight other patients suffering from an acute exacerbation of chronic bronchitis, but the mixed venous oxygen tension was very similar in both groups. This largely arose from the smaller arteriovenous difference of oxygen content in the bronchitic cases, presumably due to their higher cardiac output, associated with raised arterial CO₂ tensions. Oxygen therapy (60-90% for pulmonary oedema, 30% for the bronchitics) raised the mixed venous oxygen tensions to a similar level in both groups. We suggest that the major need for oxygen therapy lies in patients who maintain their oxygen consumption but show a reduction in mixed venous tension when breathing air. Although partial correction of arterial hypoxaemia is adequate in chronic bronchitis—in which the cardiac output is maintained—high concentrations of oxygen are necessary in pulmonary oedema, in which the cardiac output is low.     

CORRECTION OF ANOMALOUS VENOUS RETURN FROM THE RIGHT LUNG TO THE INFERIOR VENA CAVA (SCIMITAR DEFORMITY)

Anomalous pulmonary venous drainage to the inferior vena cava is a rare congenital cardiac defect. Oxygenated blood from the right lung enters the right atrium resulting in a left-to-right shunt. Because the radiographic shadow of the anomalous vein resembles a curved saber, this defect has been called the "scimitar" deformity. From 1958 through June 30, 1975, 11 patients underwent surgical correction of this anomaly at our institution with 10 survivors. Diagnosis was made by routine roentgenography of the chest in all but one patient. Eight patients had total correction which consisted of implanting the anomalous vein into the right atrium, opening the interatrial septum and applying a patch graft as a baffle to direct pulmonary venous blood into the left atrium. Five patients had associated cardiac defects which were also repaired. Three patients underwent pneumonectomy and all survived. The only operative death occurred in a 5-year-old female with an atrial septal defect and endocardial cushion defect. We believe the existence of a large left-to-right shunt justifies surgical intervention. The prognosis appears to depend upon the presence of other cardiac or pulmonary anomalies.     

Pulmonary oedema without critical increase in left atrial pressure in acute myocardial infarction.

Twelve patients with acute myocardial infarction and radiological evidence of pulmonary oedema were observed in whom the left atrial pressure, measured indirectly as pulmonary artery end-diastolic pressure, was not critically increased (range 5-12 mm Hg with reference to sternal angle). Eight of the patients had been treated with frusemide, but only six had responded: hence in at least half of the series diuresis could not account for the anomalous finding. Six patients with low cardiac output were given infusions to expand plasma volume. Appreciable increments in mean values for cardiac index (1.6 to 2.0 1/min/m2), stroke index (18 to 23 ml/beat/m2), mean arterial pressure (65 to 86 mm Hg), and pulmonary artery end-diastolic pressure (8 to 15 mm Hg) were recorded. This group, and the remaining six patients with higher cardiac output, survived to leave hospital. Delay in radiographic clearing after a fall of left atrial pressure was a possible explanation for the relatively low pulmonary artery end-diastolic pressures, especially in the patients treated successfully with diuretics. Other mechanisms, such as alterations in pulmonary vascular permeability, might also have contributed to the syndrome. Pulmonary oedema without a critical increase in the left atrial pressure is unusual in acute myocardial infarction but the therapeutic implications are important. Withdrawal;of diuretics may be indicated, and in some cases expansion of plasma volume may lead to striking clinical improvement.     

Policy for early discharge after acute myocardial infarction.

Simple criteria were used to select a low-risk group of patients after acute myocardial infarction. The criteria depended on the presence or absence of diabetes, pulmonary oedema, serious rhythm disorders, and recurrent cardiac pain. Patients in the low-risk category with a suitable home environment were discharged from hospital after five to seven days (mean 6.2 days); they constituted 47% of the 267 hospital survivors over 18 months. Mortality in the selected patients was 2.4% at six weeks and 7% at one year. Most complications preventing early discharge were identified on the first day. Provisional selection for a short hospital stay was made after two days, and 76% of those judged suitable at 48 hours remained free of complications. Early selection of a low-risk category is justifiable and of practical value, though subsequent events will delay discharge for some patients. All patients who died in hospital or within two weeks after infarction had developed overt complications by the end of the fourth day. The results suggest that a policy of hospital discharge after four days would be justifiable for a low-risk group selected by the present criteria.     

Cerebral haemorrhagic infarction in young patients with hereditary protein C deficiency: evidence for "spontaneous" cerebral venous thrombosis.

Among 53 patients with hereditary protein C deficiency belonging to 20 families three women were encountered who, aged 27, 34, and 38 respectively, had had cerebral haemorrhagic infarction, probably due to intracranial venous thrombosis. All three had also had venous thrombosis of the leg and pulmonary embolism either before or after their cerebral infarction. One patient sustained cerebral infarction while receiving an oral contraceptive, but infarction in the two others occurred "spontaneously." One patient also had an intraventricular and subarachnoid haemorrhage during the induction phase of coumarin treatment, which was assumed to have resulted from haemorrhagic infarction of the chorioid plexus, analogous to coumarin provoked haemorrhagic skin necrosis in protein C deficiency. Hereditary protein C deficiency should be considered in young patients with acute or subacute cerebral symptoms, especially if they have a family or personal history of venous thromboembolism.     

X-ray characterization of changes of the lungs in juvenile rheumatoid arthritis

The results of chest x-ray were analyzed in 66 pediatric patients with juvenile rheumatoid arthritis (JRA). X-ray signs of pneumofibrosis were revealed in 37 (56%) patients. Besides, rare pulmonary changes (emphysema, rheumatic nodules, infiltrates) were detected in the JRA patients. The absence of clinical symptoms in the presence of x-ray changes necessitates the performance of chest x-ray in JRA for early detection of the pulmonary symptoms of this disease.     

Pleuropulmonary manifestations of hepatic amebiasis.

Pleuropulmonary manifestations of hepatic amebiasis occurred in 30 patients; 18 (60%) presented with at least 1 pulmonary complaint and 10 (33%) had multiple pulmonary symptoms. In 14 patients (47%), abnormalities were found on examination of the chest. In 16 chest roentgenograms (53%), there was at least 1 abnormality: right-sided pleural effusion (9 patients) and elevated right hemidiaphragm (8 patients) were the most common. All patients were treated with metronidazole (Flagyl) and had resolution of the amebic liver abscess and pulmonary disease. Pleuropulmonary disease is a common complication of amebic liver abscess. The clinical presentation and chest roentgenograms are virtually diagnostic and obviate the need for invasive procedures to confirm the diagnosis. Pleuropulmonary disease resolves with amebicidal treatment of the hepatic abscess.     

Intermittent high altitude hypoxia - induced structural changes in the pulmonary myocardium in young mice

Seven-day-old mice, strain H, were exposed to intermittent high altitude hypoxia (IHA) in a barochamber (7,000 m, 4 h/day, 5 days a week); a total number of exposures was 10. It has been shown that the layer of cardiac musculature in the adventitia of the pulmonary veins, the so-called pulmonary myocardium, reacts to IHA hypoxia by enlargement even sooner than the right ventricular myocardium. The average thickness of the layer of pulmonary myocardium was significantly greater in animals exposed to IHA hypoxia as compared with the controls. Furthermore, IHA hypoxia induces the extension of the pulmonary myocardium to the periphery of the pulmonary venous bed. Ultrastructural investigation of the pulmonary myocardium in hypoxic animals revealed the presence of unoriented myofilaments in the peripheral myofibril-free sarcoplasma, increase in the number of ribosomes and appearance of profiles of granular endoplasmic reticulum. Our data provide quantitative support for the hypothesis that it is not only the contraction of pulmonary arteries, but also venoconstriction which contribute to the hypoxic pressure response in mice.     

Radiologic diagnosis of pathologic pulmonary changes in ischemic heart disease]

Combined chest x-ray investigation was performed in 187 CHD patients. Different pulmonary changes were noted in postinfarction and atherosclerotic cardiosclerosis as a result of congested effects in lesser circulation: they depended upon a stage of disturbed circulation (the more circulatory decompensation was noticeable, the more marked were changes in lesser circulation). Pulmonary and cardiac changes in patients with postinfarction cardiosclerosis were more frequent and marked.     

Mechanical Complications of Myocardial Infarction—Radiologic Aspects

Left ventricular aneurysm, interventricular septal defect and acute mitral valve incompetence due to papillary muscle damage are three mechanical complications which cause intractable heart failure following myocardial infarction. In each case surgical intervention can result in dramatic improvement of congestive heart failure.A hemodynamically significant left ventricular aneurysm enlarges the cardiac silhouette and frequently causes a localized protrusion as seen radiographically. Cardiac fluoroscopy will disclose an abnormal pulsation of the left ventricular border. The left ventricular angiogram establishes the diagnosis, reveals the extent of the aneurysm and may disclose a filling defect in the aneurysmal sac due to the presence of mural thrombus. Coronary arteriography shows occlusion of a major vessel, most commonly the anterior descending branch of the left coronary artery.Ischemic perforation of the interventricular septum and acute mitral incompetence due to severe papillary muscle damage both cause severe heart failure shortly after myocardial infarction. A similar pansystolic murmur accompanies both conditions, and differentiation between the two is rarely possible on the basis of the electrocardiogram or x-ray film of the chest. Ventricular cardiac catheterization and left ventricular angiocardiography are required for a correct diagnosis.     

Haemodynamic patterns in ST-elevation myocardial infarction: incidence and correlates of elevated filling pressures

Objectives. We sought to study the incidence and clinical correlates of elevated filling pressures in ST-elevation myocardial infarction (STEMI) patients, without physical signs of heart failure and treated with primary coronary angioplasty. Background. Haemodynamic data, as measured with a Swan-Ganz catheter, are not routinely obtained in STEMI patients. At admission, low blood pressure, increased heart rate, sweating, increased respiration rate, rales, oedema, and a third heart sound are indicative of heart failure. Methods. All consecutive STEMI patients were monitored by a Swan-Ganz catheter and central venous pressure (CVP), pulmonary capillary wedge pressure (PCWP), pulmonary artery pressure (PAS) and cardiac index (CI) were measured. To investigate the clinical correlates of the haemodynamic status patients were classified according to previously defined haemodynamic criteria. Results. We studied 90 patients, aged 60.5±13.1 year, 76% were male. Mortality at 30 days was 2/90 (2.2%). Patients with impaired haemodynamics presented later and had larger myocardial infarct sizes. CVP, PCWP and PAS were above normal in 36 (40%) patients. Conclusion. A large proportion of STEMI patients without physical signs of heart failure have elevation of right- as well as left-sided cardiac filling pressures. (Neth Heart J 2007:15:95-9.)     

The x-ray picture of pulmonary circulation in the course of acute myocardial infarct

A study was made of the time course of lesser circulation (LC) in 80 patients with acute transmural myocardial infarction and in 20 patients with chronic coronary heart disease with the help of chest x-ray. A possibility of preclinical detection of left ventricular insufficiency was confirmed. The capacity of roentgenography to reflect objectively the time course of LC disorder and its correlation with primary determination of a degree of changes, age, cardiac sizes, the expression of aortic atherosclerosis, pleurocardiac reactions and site of myocardial infarction were defined.     

Pneumothorax resulting from subclavian puncture: a complication of permanent pacemaker lead implantation

Pneumothorax is a mild complication during pacemaker lead implantation using the subclavian puncture technique. We report on five-year experience in 433 pacemaker lead implantation procedures in 379 patients. The cephalic vein route was solely used in twelve patients. Three procedures were performed over time in four patients and one patient needed four repetitive punctures for pacemaker lead implantation and replacement. Thus 421 punctures were carried out in 367 patients. Eleven case of pneumothorax were observed: in eight patients (1.9%) a partial pneumothorax occurred and in three patients (0.7%) the pneumothorax was nearly complete. In the latter patients a chest tube was inserted and hospital admission was prolonged for 3, 6 and 6 days, respectively. Old age with a corresponding abnormality in the form of chest deformation were predominantly found in the patients with this type of complication.     

Haemodynamic effects of salbutamol in patients with acute myocardial infarction and severe left ventricular dysfunction.

The haemodynamic effects of salbutamol infusions at rates of 10,20, and 40 micrograms/min were measured in 11 patients with acute myocardial infarction complicated by left ventricular failure. Four patients also had cardiogenic shock. Consistent increases were observed in cardiac outputs at all doses (up to 56% at 40 micrograms/min), while the mean systemic arterial pressure fell slightly (average 5 mm Hg), implying a reduction in peripheral vascular resistance. Changes in right atrial pressure and indirect left atrial pressure (measured as pulmonary artery end-diastolic pressure) were small and not significant. Analysis of data from individual patients showed that the greatest increment in cardiac output was reached at 10 micrograms/min in two cases, 20 microgram/min in three, and 40 micrograms/min in the remaining six. Heart rate at these doses increased by an average of only 10 beats/min. Salbutamol failed to reduce left ventricular filling pressure and cannot be recommended for the treatment of pulmonary oedema in acute myocardial infarction. The increase in cardiac output, however, was considerable, so that the drug may be important in the management of low-output states. This action is probably a result of peripheral arteriolar dilatation (itself a result of beta 2-adrenoreceptor stimulation) and is achieved with little alteration in the principal determinants of myocardial oxygen requirement.     

Fatal ischaemic brain oedema after early thrombolysis with tissue plasminogen activator in acute stroke.

Two patients with acute major, disabling cerebral infarction with presumed middle cerebral artery occlusion were treated with the clot specific thrombolytic agent tissue plasminogen activator roughly three and a half hours after the onset of symptoms. Both patients had a normal computed tomography (CT) scan before treatment. No appreciable systemic bleeding complications occurred, apart from bruising. One patient had bleeding into the subarachnoid space from a microscopic angioma, which was found at necropsy. Haematological monitoring of the two patients showed pronounced fibrinogenolysis and alpha 2 antiplasmin consumption in one. One patient showed transient improvement during the infusion. In both cases extensive infarction, partly haemorrhagic in one, with massive concomitant oedema was found on repeated CT. Both patients deteriorated and eventually died as a consequence of transtentorial herniation. In the one patient who came to necropsy a moderate, probably pre-existing smooth stenosis of the ipsilateral carotid artery was found, all cerebral vessels being patent. It is concluded that thrombolytic treatment with a clot specific agent such as tissue plasminogen activator started three to four hours after a major ischaemic stroke may be hazardous, not because of haemorrhagic transformation of the original ischaemia but because early reperfusion may promote massive, potentially fatal cerebral oedema.     

Sequential growth of fetal sheep cardiac myocytes in response to simultaneous arterial and venous hypertension

While the fetal heart grows by myocyte enlargement and proliferation, myocytes lose their capacity for proliferation in the perinatal period after terminal differentiation. The relationship between myocyte enlargement, proliferation, and terminal differentiation has not been studied under conditions of combined arterial and venous hypertension, as occurs in some clinical conditions. We hypothesize that fetal arterial and venous hypertension initially leads to cardiomyocyte proliferation, followed by myocyte enlargement. Two groups of fetal sheep received intravascular plasma infusions for 4 or 8 days (from 130 days gestation) to increase vascular pressures. Fetal hearts were arrested in diastole and dissociated. Myocyte size, terminal differentiation (%binucleation), and cell cycle activity (Ki-67[+] cells as a % of mononucleated myocytes) were measured. We found that chronic plasma infusion greatly increased venous and arterial pressures. Heart (but not body) weights were approximately 30% greater in hypertensive fetuses than controls. The incidence of cell cycle activity doubled in hypertensive fetuses compared with controls. After 4 days of hypertension, myocytes were (approximately 11%) longer, but only after 8 days were they wider (approximately 12%). After 8 days, %binucleation was approximately 50% greater in hypertensive fetuses. We observed two phases of cardiomyocyte growth and maturation in response to fetal arterial and venous hypertension. In the early phase, the incidence of cell cycle activity increased and myocytes elongated. In the later phase, the incidence of cell cycle activity remained elevated, %binucleation increased, and cross sections were greater. This study highlights unique fetal adaptations of the myocardium and the importance of experimental duration when interpreting fetal cardiac growth data.     

How long should patients with suspected myocardial infarction be under observation in hospital?

Out of 368 patients admitted to hospital for chest pain and suspected acute myocardial infarction, 267 were discharged within 24 hours on the basis of the clinical picture, electrocardiogram, and serum activities of aspartate transaminase, alpha-hydroxybutyrate dehydrogenase, and creatine phosphokinase. The patients were followed up for 28 days, during which 17 were readmitted, two of them twice and one three times. Two of the patients were readmitted with non-fatal acute myocardial infarction, and two died. The patients had been primarily divided into two groups: those admitted with presumably non-coronary chest pain (77 patients) formed group 1 and those with obvious coronary chest pain (190 patients) group 2. Both deaths occurred in patients in group 2 but the incidences of events during the follow-up period were otherwise similar in the two groups, and some patients in both groups may have had small acute myocardial infarctions when first admitted. The decision to keep in hospital or discharge a patient with chest pain of recent onset can be made within 24 hours of admission. To discharge the patient acute myocardial infarction need not necessarily be excluded and conventional tests are enough to enable a decision to be made.     

Study of the management of suspected cardiac infarction by British immediate care doctors.

A study of the management by immediate care general practitioners of 511 patients suspected of suffering from acute myocardial infarction showed that the median time of arrival after the onset of chest pains was 60.2 minutes. One hundred and eleven patients died of cardiac infarction within 48 hours of the onset of chest pain; 23 died in the presence of the general practitioner.     

Infarct-induced wall motion abnormalities in aortocoronary bypass patients: Correlation with electrocardiographic, enzymatic, and scintigraphic diagnostic criteria

Gated isotope ventriculograms performed 7 to 12 days postoperatively in 50 aortocoronary bypass patients with perioperative myocardial infarction (POMI) were compared with preoperative contrast ventriculograms. The diagnosis of POMI was based on serial electrocardiograms (EKGs), cardiac enzyme studies, and (99m)Tc-pyrophosphate (PYP) scintigraphy. Seven patients exhibited no new regional wall motion abnormalities. Nine had new areas of localized hypokinesis. The remaining 34 demonstrated localized akinesis or dyskinesis; 12 of these also exhibited a greater than 20% decrease in ejection fraction. The severity of the postoperative wall motion abnormality was paralleled by the intensity of PYP accumulation but not necessarily by the degree of cardiac enzyme elevation. Because they occurred in only 62% of patients, new Q waves were considered an insensitive indicator of POMI. Our study revealed that POMI frequently produces significant changes in left ventricular kinetics. Of the standard techniques utilized, the PYP scan had the greatest predictive value.