Streptococcal mural endocarditis and myocardial abscess occurring in a left ventricular aneurysm--case report and review.

Infection of the mural endocardium within a left ventricular aneurysm without valvular involvement is exceedingly rare. The presenting clinical features can be non-specific, and a high index of suspicion is required for its diagnosis. Delay in diagnosis invariably leads to a fatal outcome. Although no controlled studies are available to guide therapy and management of these patients, appropriate antibiotic therapy and early surgical resection of the infected ventricular aneurysm remain the cornerstone of therapy.

The effect of angiotensin converting enzyme inhibition on myocardial function and blood pressure after coronary artery bypass surgery--a randomised study.

OBJECTIVE: To investigate the effect of 6 weeks' pre-operative treatment with the angiotensin converting enzyme inhibitor, quinapril, on left ventricular function when measured 3 months after coronary artery bypass graft surgery and to examine the safety of such treatment. PATIENTS AND METHODS: Patients (96) [86 males, 10 females; mean age 61 years] with chronic stable angina, on the waiting list for coronary artery bypass graft surgery, underwent measurement of left ventricular function by resting radionuclide ventriculography. Patients were then randomised to quinapril 20 mg once daily or placebo in a double-blind fashion, in addition to existing anti-anginal therapy and this regimen was continued for up to 6 weeks prior to operation. Measurement of left ventricular function was repeated 3 months following surgery, after recommencement of pre-surgery anti-anginal therapy for 1 week. Effects on systemic vascular resistance (SVR) during bypass were calculated from perfusion records and vasoconstrictor use during operation was documented. The safety of the addition of quinapril to the anti-anginal regimen was assessed by measurement of systemic blood pressure (BP) after the first dose of study medication, measurement of intra-operative BP, administration of inotropes and any intra-operative complications. RESULTS: There was no difference between treatment groups in the pre-study left ventricular ejection fraction (mean (S.D.); 54.9 (13.8)% versus 55.6 (13.2)%, quinapril versus placebo, respectively), or 3 months after surgery (58.1 (13.6)%, versus 56.9 (12.6)%, quinapril versus placebo, respectively). Left ventricular ejection fraction 3 months after surgery did not change significantly from pre-treatment in either group (2.8 (10.7)% and 1.5 (10.1)%; quinapril and placebo, respectively). There was no first-dose hypotension (systolic BP < 100 mmHg). The intra-operative BP and the SVR during bypass in the two treatment groups were not significantly different. The ischaemic time (mean = 56 min) and the use of inotropes were the same in both groups and there was no mortality. CONCLUSIONS: Angiotensin converting enzyme inhibitor treatment before coronary artery bypass graft surgery does not have a significant beneficial effect on left ventricular function following coronary artery bypass graft surgery. Angiotensin converting enzyme inhibition, administered in addition to anti-anginal therapy, does not cause first-dose hypotension or increase morbidity or mortality and can safely be used in patients with coronary heart disease prior to coronary artery bypass graft surgery.

Methcathinone intoxication in the rat: abrogation by dextrorphan.

STUDY OBJECTIVE: Methcathinone, a designer drug, has high abuse liability. In this study we characterized acute methcathinone toxicity in rats, attempting to determine whether the excitatory amino acid receptor antagonist dextrorphan can antagonize methcathinone intoxication. METHODS: Intoxication was produced with IV methcathinone infusion (5 mg/kg/minute; 100 mg/mL) in conscious rats. We studied pretreatment, in which dextrorphan or vehicle was injected 30 minutes before methcathinone infusion. In a second protocol, dextrorphan or saline solution was given immediately after the onset of convulsions. RESULTS: Methcathinone caused tachycardia (maximal increase, 131 +/- 10 beats/minute), hyperthermia (+2.3 degrees C), convulsions, and cardiorespiratory collapse in vehicle-pretreated rats (n = 9). Death occurred after 32.0 +/- 1.1 minutes of infusion. Dextrorphan pretreatment (25 mg/kg; n = 7) significantly reduced hyperthermia (+.1 degree +/- .3 degree C) and tachycardia and increased the convulsive (dextrorphan, 134 +/- 9 mg/kg; vehicle, 67 +/- 4 mg/kg) and lethal doses (dextrorphan, 204 +/- 9 mg/kg; vehicle, 160 +/- 5 mg/kg). Dextrorphan, given immediately after the initial methcathinone convulsion, reduced hyperthermic and tachycardic responses but not the lethality of methcathinone. CONCLUSION: Blockade of excitatory amino acid receptors by dextrorphan minimizes acute methcathinone intoxication.

Anomalous papillary muscle as a cause of left ventricular outflow tract obstruction in an adult.

Left ventricular outflow tract obstruction may be caused by abnormalities of the various structures comprised by the outflow tract. Hypertrophic cardiomyopathy is one of the more common causes, but many are rare anomalies, a collection of which we have compiled. We present a case of left ventricular outflow tract obstruction mimicking aortic stenosis in an adult. This was found to be due to abnormal insertion of a hypertrophied papillary muscle, successfully corrected by mitral valve replacement.

Histological abnormalities of muscle from limb, thorax and diaphragm in chronic heart failure.

The aim of the study was to compare histological findings in limb and respiratory muscles from control subjects and patients with heart failure of two different aetiologies. Biopsies of the quadriceps femoris, strap, diaphragm and pectoralis major muscles were taken from each group. The control subjects all had normal left ventricular function, and comprised seven undergoing surgical ablation of electrical pathways and 10 undergoing coronary artery surgery. The heart failure group had severely impaired left ventricular function, and were undergoing cardiac transplantation in all except one case. Ten patients with idiopathic dilated cardiomyopathy and seven with heart failure of ischaemic origin were studied. Conventional histochemical techniques and specific anti-myosin immunofluorescent stains were used. There were no consistent differences in fibre type prevalence or diameter between the groups. There were no important histological abnormalities in the two control groups. There were minor/major changes in four of seven patients with ischaemic heart failure but no major abnormality, whilst in the dilated cardiomyopathy group there were five of 10 patients with minor/major changes and three of 10 with major abnormalities (P < 0.001 vs controls). A variety of changes were seen in both groups of heart failure subjects. These were more marked in the dilated cardiomyopathy than ischaemic group, and suggest the presence of fibre type regeneration and/or transformation. Amongst the findings were tubular aggregates, internalization of nuclei, bizzare staining of myosin and staining of neonatal myosin (seven of 14) and the presence of cores (five of 14). Such changes were more prominent in the diaphragm than in the other muscles. In conclusion, histological abnormalities are present in the limb and respiratory muscles from subjects with heart failure. The changes are most marked in subjects with idiopathic dilated cardiomyopathy, suggesting that there may be a generalized cardiac and skeletal myopathy in these subjects. The presence of histological abnormalities in the respiratory muscles may contribute to the pathogenesis of dyspnoea in heart failure.

Reduced contraction and altered frequency response of isolated ventricular myocytes from patients with heart failure.

BACKGROUND: Previous work has failed to demonstrate reduced maximal contraction of isolated ventricular myocytes from failing human hearts compared with nonfailing control hearts. The effect of alterations in stimulation frequency and temperature on the contraction of isolated ventricular myocytes has been investigated. Left ventricular myocytes were isolated from the hearts of patients with severe heart failure undergoing heart transplantation and compared with myocytes isolated from myocardial biopsies from patients with coronary disease but preserved left ventricular systolic function or from myocytes from rejected donor hearts. METHODS AND RESULTS: Myocytes were exposed to either a maximally activating level of extracellular calcium at 37 degrees C or to 2 mmol/L calcium at 32 degrees C. There was no significant difference in the contraction amplitude between myocytes from failing and nonfailing hearts at 0.2 Hz. With increasing stimulation frequency, there was a reduction in contraction amplitude in cells from failing hearts relative to control hearts in both maximal calcium from 0.33 Hz (4.5% versus 6.6%) to 1.4 Hz (3.9% versus 8.8%) (ANCOVA, P < .001) and at 2 mmol/L calcium from 0.50 Hz (2.3% versus 3.5%) to 1.4 Hz (1.8% versus 3.9%) (ANCOVA, P < .001). The time to peak contraction and the times to 50% and 90% relaxation were prolonged in myocytes from failing hearts at stimulation rate of 0.2 Hz (P < .01), but only the time to 50% relaxation was prolonged at 1.0 Hz (P < .05). CONCLUSIONS: Reduced contraction, slowed relaxation, and impaired frequency response occurring at the level of the individual ventricular myocyte can be demonstrated in human heart failure. This demonstrates that disruption of myocyte function can contribute to both the systolic and the diastolic abnormalities that occur in the failing human heart.

Unidentified retained left atrial myxoma: intra-operative detection by trans-oesophageal echocardiography.

A 73-year-old woman underwent surgery for removal of a large left atrial myxoma diagnosed by transthoracic echocardiogram. At operation a large tumour was removed, and the left atrium and atrial septum closed. Trans-oesophageal echocardiography prior to weaning from cardiopulmonary bypass revealed that a smaller tumour, which had not been detected by visual inspection or palpation, remained within the left atrium. This was removed through the atrial septum, and the operation completed uneventfully. The patient made a full recovery.

Ultrastructural analysis of skeletal muscle. Microvascular dimensions and basement membrane thickness in chronic heart failure.

Chronic heart failure (CHF) is characterized by increased systemic vascular resistance and diminished blood flow to exercising skeletal muscle. The pathogenesis of the increased resistance is not known, and may be due to muscle atrophy, functional abnormalities of resistance vessels or to structural changes in the microcirculation such as endothelial cell swelling. We have compared the ultrastructure of the microvasculature in needle biopsies of the quadriceps muscle from seven control subjects with normal left ventricular function to 10 patients with moderate or severe heart failure, optimally treated and without evidence of fluid overload. Samples were processed for ultrathin sectioning using ruthenium red as a specific basement membrane (BM) stain. Electron micrographs were taken of 10 transversely cut capillaries from each specimen. The total cross-sectional area of the vessels and the area of the endothelium was determined, and the short axis diameter was measured as an index of vessel diameter. The BM thickness was calculated from the mean of six readings around the periphery of the vessel. The short axis diameter in the two groups was not significantly different (controls 3.37 +/- 0.21 microns, CHF 3.56 +/- 0.37 microns, mean +/- 1SD). No difference in total cross-sectional area (controls 11.64 +/- 1.86 microns 2, CHF 13.56 +/- 2.78 microns 2) or area of the endothelium (controls 4.90 +/- 1.18 microns 2, CHF 6.00 +/- 1.58 microns 2) was observed. The thickness of the BM was marginally increased in subjects with CHF when compared to control subjects (0.31 +/- 0.077 microns vs 0.246 +/- 0.047 microns, P = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

The Wolff-Parkinson-White syndrome: the cellular substrate for conduction in the accessory atrioventricular pathway.

The longstanding quest for the anatomical basis of the Wolff-Parkinson-White syndrome has left many unanswered questions. The ultrastructural morphology of the myocytes comprising accessory atrioventricular pathways, which are capable of rapid and variable conduction, is central to understanding the development and behaviour of this congenital anomaly, but remains unknown. Examination of three surgically resected pathways was performed to determine their underlying cellular morphology and the pattern of intercellular coupling, by correlative light microscopy, electron microscopy and confocal scanning laser microscopy combined with immunohistochemical localization of the cardiac gap-junctional protein, connexin43. Two left-sided pathways were composed of myocardium of 'normal working ventricular' type. The right-sided pathway was composed almost entirely of highly abnormal myocytes characterized by aberrant myofibril organisation, with a lack of A-band material and abnormal mitochondria, but normal intact intercalated disks no different from those seen in left-sided pathways. The gap junctions of all pathways were composed of connexin43 distributed as in ventricular myocardium, and not as found in atrial or atrioventricular nodal tissues. While myocytes of abnormal structure were present in one of the accessory atrioventricular pathways examined, all pathways had morphologically normal gap junctions, the structures responsible for efficient intercellular coupling, with a pattern of distribution suggestive of working ventricular myocardium.

Urethane anesthesia reverses the protective effect of noncompetitive NMDA receptor antagonists against cocaine intoxication.

The present experiments examined whether pretreatment with the noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonists, MK-801 and dextrorphan, could antagonize cocaine-induced convulsions and lethality in conscious Sprague-Dawley (SD) rats and whether urethane anesthesia alters the observed interactions. Conscious, restrained male SD rats received continuous i.v. infusions of cocaine hydrochloride (1.25 mg/kg.min) until convulsions and death occurred. Cocaine doses of 21.2 +/- 1.8 and 29.5 +/- 2.5 mg/kg caused convulsions and death, respectively, in saline treated rats (n = 8). Convulsions were absent in MK-801 (1 mg/kg, i.v.; n = 8) pretreated rats; the lethal cocaine dose was 44.0 +/- 2.7 mg/kg (p < 0.05). In contrast, urethane anesthesia (1.2 g/kg, i.p.) decreased the dose of cocaine required to cause toxicity, compared to that in saline controls (24.8 +/- 0.8 mg/kg, n = 13), in MK-801 (2.0 +/- 0.3, n = 7; p < 0.01) and in dextrorphan mg/kg, n = 13), in MK-801 (2.0 +/- 0.3, n = 7; p < 0.01) and in dextrorphan (25 mg/kg, i.v.; 13.1 +/- 1.4, n = 6; p < 0.01) pretreated rats. Pressor responses with little change in heart rate were evident during cocaine infusion in vehicle pretreated rats. Bradycardiac responses were noted to cocaine in groups following NMDA receptor blockade. Reversal of the pressor response to cocaine was noted in MK-801 pretreated animals, while dextrorphan pretreatment moderated cocaine-induced increases in blood pressure. Ventilatory support protected against cocaine lethality in urethane anesthetized rats, indicating that respiratory failure is the proximate cause of death with cocaine infusion. However, artificially ventilated rats, pretreated with MK-801, were more sensitive (lethal cocaine dose, 76.6 +/- 8.0 mg/kg, n = 5) than vehicle pretreated rats (129.4 +/- 15.8 mg/kg, n = 6), indicating that MK-801 may increase both the respiratory and the cardiac toxicity of cocaine in urethane anesthetized rats. Interactions between NMDA receptors and cocaine are modified by urethane anesthesia.

Strut fracture with Björk-Shiley 70 degrees convexo-concave valve. An international multi-institutional follow-up study.

Between 1980 and 1983, 831 Björk-Shiley 70 degrees convexo-concave prosthetic heart valves were implanted at five institutions in Sweden, Germany. The Netherlands, and Canada. As of January 1991, there were 34 outlet strut fractures occurring from 0.2 to 10.1 years (median = 4.6 years) after implantation. In addition, there were 28 sudden, unexplained deaths. The mortality after strut fracture was 84%. The mortality after emergency valve replacement for strut fracture was 50%. The 10-year actuarial fracture rate (standard error) was 10.5 (2.4)% for large (29-33 mm) valves vs. 3.3 (1.2)% for 21-27 mm valves (P less than 0.001). Within valve size groups, fracture rates for aortic and mitral valves were similar. Cox regression analysis found only valve size to be significantly associated with strut fracture. There is a further subgrouping of the valves according to the manufacturer: group I are the earlier large 29-33 mm) valves; group II are the later large valves; group III are the small size (21-27 mm) valves. The risk of strut fracture was highest in group I (12.3% at 10 years) with an approximatively constant hazard (1.4% per year). A comparison was made with a statistical model incorporating all cases reported to the manufacturer. This model estimates fracture rates approximately 63%-73% of those found in the present study. These findings lead us to recommend that group I patients should be considered for elective reoperation on an individual basis, giving careful attention to risk factors and contraindications.

Coronary artery spasm during mitral valve replacement.

Coronary artery spasm has been reported as a cause of myocardial ischaemia and necrosis during and after coronary revascularisation [1-4, 9, 11, 13, 14], but not after valve replacement. We report a case in which profound myocardial ischaemia after mitral valve replacement leading to difficulty in terminating cardiopulmonary bypass was caused by coronary vasospasm. It is suggested that coronary vasospasm has to be considered among the causes of myocardial insufficiency after cardiopulmonary bypass, even in the absence of coronary artery disease, and effective treatment may be obtained by coronary vasodilating drugs.

Mitral stenosis in systemic lupus erythematosus. Successful management by mitral valve replacement.

A female Caucasian with a history of 18 years of systemic lupus erythematosus (SLE) developed symptoms and signs of mitral stenosis, but had no history of rheumatic fever. Investigations confirmed severe stenosis, and the diseased valve was replaced by a pericardial xenograft. Histological examination was compatible with steroid-modified Libman-Sacks endocarditis. She remains well 24 months postoperatively.

Irregularly shaped small shadows on chest radiographs, dust exposure, and lung function in coalworkers' pneumoconiosis.

The predominant shapes of small opacities on the chest radiographs of 895 British coalminers have been studied. The aims were to determine whether irregular (as distinct from rounded) small opacities can be identified reproducibly, whether their occurrence is related to dust exposure, and whether they are associated with excess prevalence of respiratory symptoms or impairments of lung function. Six of the doctors responsible for regular radiological surveys of all British coalminers each classified all 895 radiographs twice and independently, using the International Labour Organisation's 1980 classification system. The majority view was that 39 films showed predominantly irregular small opacities, 131 showed predominantly small rounded opacities, and 587 showed no small opacities. Readers' opinions varied about the presence and shapes of shadows on the other 138 films. In general, consistency between readers (and within readers on repeated viewings) was satisfactory. The occurrence and profusion of irregular shadows were related significantly both to the men's ages and additionally to their cumulative exposure to respirable coalmine dust as determined from 15 years' dust monitoring close to where the miners had worked. For any given level of exposure, the average level of profusion of the small irregular opacities was less than the corresponding profusion of small rounded opacities. The prevalence rates of chronic cough and phlegm, and of breathlessness, were higher in those with small irregular opacities than in those with no small opacities (category 0/0), but the differences were not statistically significant after adjustment for other factors including smoking habits. The presence of irregular (but not rounded) small shadows was associated with an impairment in respiratory function averaging about 190 ml deficits in both FEV1 and FVC. These deficits were not explicable in terms of the men's ages, body sizes, and smoking habits and they were in addition to the lung function losses attributable to the miners' dust exposure as such. It is concluded that the presence and profusion of small irregular opacities should be taken into consideration when assessing the severity of coalworkers' simple pneumoconiosis.

Compartment syndrome and intraaortic balloon.

Intraaortic balloon (IAB) is a well accepted and useful therapeutic option; the complications reported with it's use are varied. We have observed 4 patients over a period of 6 years, who developed swollen tender calves and loss of sensation and/or function, yet who retained a warm limb with palpable peripheral pulses during or immediately after IAB pumping. At fasciotomy, they had bulging ischemic muscles. We hypothesize that this is compartment syndrome following temporary or partial ischemia due to balloon placement. We have prospectively studied 13 patients by measuring the pressure in the anterior compartment of the lower limb using the slit catheter technique. In 11 of these patients with no evidence of complications, pressure measurements remained below 7 mmHg. In one patient showing signs consistent with compartment syndrome, pressures up to 35 mmHg were recorded and at fasciotomy, the diagnosis was confirmed. A second patient with signs suggestive of compartment syndrome, had pressures below 15 mmHg. This patient was treated conservatively with resolution of the condition. Compartment syndrome after IAB placement has only been rarely described. We believe this is due to inadequate diagnosis and that slit catheter pressure measurements are a valuable tool in its management. We encountered no complications associated with the technique.

Evaluation and treatment of anterior knee pain using eccentric exercise.

Various authors have indicated that muscle imbalances might lead to knee pain and the potential for knee injury during sports. However, few reports have been published to substantiate such a hypothesis. But in all of the existing studies, only concentric torque measurements were evaluated. The purpose of the present study was to document any torque deficiencies which might be present during eccentric exercise in patients with knee pain. Of 130 patients with various knee disorders, 41 demonstrated a suppression in torque production during the eccentric exercise and generally in the portion of the range of movement between 30 degrees and 60 degrees of knee flexion (P less than 0.05). These individuals fit the criteria for anterior knee pain syndrome and demonstrated remarkable improvement after training 3 times/wk at concentric-eccentric exercises of the knee extensors at various speeds (30 degrees, 60 degrees, and 90 degrees . s-1) on a computer-controlled dynamometer (KIN/COM). In some cases, the pain as well as their torque deficiency was relieved after only 2 wk of training, most others were relieved after 2 to 4 wk of training.

The role of echocardiography in suspected bacterial endocarditis.

We evaluated the clinical application of echocardiography (M and 2D modes) in the assessment of cardiac patients with fever and an underlying valvular abnormality in whom the diagnosis of infective endocarditis was suspected. One or more of the classic clinical features of the disease were present in 50 patients (group A). Vegetations were detected by echocardiography in 17 (47%) out of the 36 patients within this group A who had positive blood cultures. Four (28.5%) of the remaining 14 patients with unequivocal endocarditis clinically and negative blood cultures had demonstrable vegetations on ultrasound. Anatomical complications resulting from the septic process (valve destruction or detachment, aortic root abscess) were visualized in 18 (36%) of the 50 patients in group A. The clinical features of endocarditis were lacking in the other 53 patients with fever and murmur (group B). This group included 12 patients with other sources of bacteraemia besides endocarditis. Unsuspected vegetations were detected only in 2 (3.7%) out of the 53 cases. Thus echocardiography is useful in confirming the clinical diagnosis of infective endocarditis, but only rarely detects vegetations in patients who lack the characteristic clinical features of endocarditis, regardless of whether they have positive negative blood cultures.