Tetanus may be mild, moderate, severe, or inevitably fatal. Our clinical experience suggests it may be classified as severe (or, maybe, inevitably fatal) when a tetanic spasm stops respiration. Ten patients with severe tetanus were treated by the total paralysis regime (T.P.R.), consisting of tracheostomy, curarization, and intermittent positiveor positive/negative-pressure respiration. Two of the patients were saved by T.P.R. and therefore only limited effectiveness can be claimed for the regime. In inevitably fatal cases survival can be prolonged by T.P.R. so that further effects of tetanus toxin emerge. Of these, the most important appears to be direct damage to the myocardium.
Material from 334 consecutive autopsies on Orang Asli subjects performed in the University Hospital, Kuala Lumpur between May 1967 and June 1978 was examined for amyloidosis. Nine positive cases were found, all in patients above 40 years of age, giving an age-corrected incidence of about 9%. In 6 cases, amyloidosis was probably secondary to tuberculosis. The remaining 3 cases exhibited a pericollagenous distribution characteristic of primary amyloidosis. Involvement of the heart and lungs was prominent. However, there were considerable similarities in the distribution and staining properties of the amyloid in the 2 groups. Though both the heart and kidney were frequently affected, the kidney was the most common organ to give rise to clinical symptoms. Infection probably plays a major contributory role in amyloidosis in the Orang Asli.
Nineteen out of 121 consecutive cardiac biopsies from 107 patients were found to contain amyloid deposits on routine Congo red screening. Seventeen were left atrial appendages removed during mitral valvotomy for chronic rheumatic mitral valve disease while the remaining two were right atrial appendages excised during surgical repair of atrial septal defects. The distribution of amyloid deposits within the atria and their tinctorial characteristics are described. The high prevalence of atrial amyloidosis observed could not be attributed to generalized or senile amyloidosis. The possibility that this is a distinctive localized form of amyloidosis secondary to chronic heart disease is discussed.
A myopathy associated with elongated intramuscular protozoan schizonts of uncertain classification was observed in chickens in commercial farms. Of 152 affected fowls originating from 21 flocks in 12 farms, 149 were 24 weeks of age or older and 136 were broiler breeder birds. Both sexes were affected. The disease was only observed during the months of October, November and December, 1976 and 1977. The monthly mortality rate in affected adult flocks rose by 0.5% to 4% and the egg production declined by 5% to 15% during this period. Most affected birds were in good body condition or overweight. Gross lesions were usually present in all skeletal muscles and the cardiac muscle. They resembled nutritional myopathy, sarcosporidiosis, leucocytozoonosis or haemorrhagic syndrome. Microscopically visible elongated schizonts were demonstrated in skeletal muscles and the cardiac muscle in 49 of 55 birds examined histologically. The possible aetiology with respect to known parasites of muscles in fowls is discussed.
The present research is on a milky sap obtained from the Antiaris toxicaria tree (Moraceae) which is called Upas or Ipoh in Indonesia. The crude sap was administered to anesthetized rats, and changes in electrocardiogram (ECG) and systemic blood pressure was observed. Biologically and pharmacologically active components were extracted from the crude sap by means of water-acetone solution. Based on the strength of chemical qualitative detection tests of the sap extract (SE), cardiac glycosides are supposed to be the main components. The SE inhibited the Na+-, K+-ATPase (EC 3.6.1.3) which was partially purified from guinea pig heart muscle. When the SE and, concurrently, authentic ouabain were applied to isolated frog heart muscles, the fall of twitch tension was observed after the increased tension on mechanograms. These facts suggest that the main components of the milky sap are cardiac glycosides, and glycosides affect Na+, K+-ATPase activity of muscle membrane and heart muscle contraction.
The findings of autopsies performed on 35 leprosy subjects in the University Hospital, Kuala Lumpur, between January 1981 and December 1985 are presented. This is the first report based on autopsy findings from Malaysia. The patients were elderly subjects with a mean age of 74 years. Sixty-six percent had lepromatous leprosy. None had active skin lesions. The most common cause of death was pyogenic infection, particularly bronchopneumonia. Tuberculosis was noted in 25% of the cases. The other important causes of death included cardiac and renal failure. Renal lesions were evident in 71% of the cases, and the most common pathology was interstitial nephritis. Generalized amyloidosis complicated six (17%) patients.
This study examined the effects of streptozotocin-induced diabetes on blood pressure and cardiac tissue kallikrein levels in WKYR and SHR. Streptozotocin-induced diabetes caused significant (p < 0.001) increase in SBP and DBP in WKYR and SHR as compared with their respective controls. We also observed that the active cardiac tissue kallikrein levels reduced greatly (p < 0.001) in diabetic WKYR and SHR than the normal rats. These findings suggest for the first time that the cardiac tissue kallikrein formation may have a greater role in the regulation of blood pressure and cardiac function.
We investigated the cardiac tissue kallikrein and kininogen levels, left ventricular wall thickness and mean arterial blood pressure of Wistar Kyoto and spontaneously hypertensive rats with and without streptozotocin-induced diabetes. The mean arterial blood pressure was highly elevated (P<0.001) in Wistar Kyoto diabetic and spontaneously hypertensive diabetic rats as compared with their respective controls. The cardiac tissue kallikrein and kininogen levels were reduced significantly (P<0.001) in diabetic Wistar Kyoto, spontaneously hypertensive and diabetic spontaneously hypertensive compared with Wistar Kyoto control rats. In addition, the left ventricular thickness was found to be increased (P<0.001) in diabetic Wistar Kyoto and spontaneously hypertensive rats in the presence and in the absence of diabetes. Our results indicate that reduced activity of the kinin-forming system may be responsible for inducing left ventricular hypertrophy in the presence of raised mean arterial blood pressure in diabetic and hypertensive rats. Thus, the kinin-forming components might have a protective role against the development of left ventricular hypertrophy. The possible significance of these findings is discussed.
The binding characteristics of the relaxin receptor in rat atria, uterus and cortex were studied using a [33P]-labelled human gene 2 relaxin (B33) and quantitative receptor autoradiography. The binding kinetics of [33P]-human gene 2 relaxin (B33) were investigated in slide-mounted rat atrial sections. The binding achieved equilibrium after 60 min incubation at room temperature (23+/-1 degrees C) and dissociated slowly. The association and dissociation rate constants were 4.31+/-0.34x10(8) M(-1) x min(-1) and 1.55+/-0.38x10(-3) min(-1) respectively. Thus, the kinetic dissociation constant was 3.46+/-0.59 pM. Binding was saturable to a single population of non-interacting sites throughout atria, in uterine myometrium and the 5th layer of cerebral cortex. The binding affinities (pK(D)) of [33P]-human gene 2 relaxin (B33) were 8.92+/-0.09 in atrial myocardium and 8.79+/-0.04 in cerebral cortex of male rats, and 8.79+/-0.10 in uterine myometrium. Receptor densities in the cerebral cortex and atria were higher than in uterine myometrium, indicating that relaxin also has important roles in non-reproductive tissues. In male rats, treatment with 17beta-oestradiol (20 microg in 0.1 ml sesame oil s.c., 18-24 h) significantly decreased the density of relaxin receptors in atria and cerebral cortex. Identical treatment in female rats had no significant effect in atria and cerebral cortex, but it significantly increased the density of relaxin receptors in uterine myometrium. Relaxin binding was competitively displaced by porcine and rat native relaxins. Porcine native relaxin binds to the relaxin receptor in male rat atria (8.90+/-0.02), and cerebral cortex (8.90+/-0.03) and uterine myometrium (8.89+/-0.03) with affinities not significantly different from human gene 2 (B33) relaxin. Nevertheless, rat relaxin binds to the receptors with affinities (8.35+/-0.09 in atria, 8.22+/-0.07 in cerebral cortex and 8.48+/-0.06 in uterine myometrium) significantly less than human gene 2 (B33) and porcine relaxins. Quantitative receptor autoradiography is the method of choice for measurement of affinities and densities of relaxin receptor in atria, uterine myometrium and cerebral cortex. High densities were found in all these tissues. 17beta-oestradiol treatment produced complex effects where it increased the densities of relaxin receptors in uterus but decreased those in atria and cerebral cortex of the male rats, and had no effect on the atria and cerebral cortex of the female rats.
The present investigation was aimed at evaluating the cardiac and total plasma kininogen levels, as well as LVWT in hypertensive and diabetic rats. STZ-induced diabetes produced a significant (P < 0.001) rise in mean arterial blood pressure (BP). The LVWT increased (P < 0.001) in SHR with and without diabetes) and diabetic WKYR. The cardiac tissue, as well as total plasma kininogen levels fell significantly (P < 0.001) in diabetic WKYR and SHR with and without diabetes compared to the control WKYR. These findings suggest that reduced kininogen levels may indicate a deficiency in kinin generation in the heart and in the peripheral circulation in diabetic and hypertensive rats. This effect may contribute to the development of LVH.
Epidemics of enterovirus 71 infections caused the rapid death of many children in Malaysia in 1997 and in Taiwan in 1998. Pulmonary edema occurred in most of the fatal cases and was considered to be neurogenic. The role of the heart was rarely investigated before. Between January 1998-January 2001, 34 consecutive patients who were admitted to the intensive care unit due to enterovirus infection were studied prospectively. Patients were divided into two groups: group I with pulmonary edema, and group II without pulmonary edema. Comparisons were made between the two groups based upon demographic, neurological, and cardiovascular manifestations. Group I consisted of 11 patients (5 boys, 6 girls; mean age, 22.8 months), and group II of 23 patients (12 boys, 11 girls; mean age, 28.8 months). There were no significant differences between the two groups in comparing sex, age, body weight, neurological severity, intracranial pressure, cell count, protein and glucose levels in cerebral spinal fluid, and blood pressure. All group I patients had left ventricular dysfunction, and their ejection fractions were significantly lower than those of patients in group II (37 +/- 11% vs. 75 +/- 6%, P < 0.001). Group I heart rates were higher than those of group II (175 +/- 24 vs. 137 +/- 25, P < 0.001). In group I, 9 patients who received conventional treatment died, and the only two survivors received left ventricular assist devices. In conclusion, the pulmonary edema of fulminant enterovirus 71 infection is associated with left ventricular failure. Left ventricular function is the major determinant of outcome. Early recognition of heart failure and aggressive cardiac intervention are life-saving. Pediatr Pulmonol. 2003; 35:263-268.
Cardiac sarcoidosis is a disease of young adults. In most cases it presents with sudden death, arrhythmias, conduction disorders, heart failure or cardiomyopathy. The authors describe two cases of myocardial involvement by sarcoidosis that lead to death of the patients. Case one was a 26-year-old Indian man who was previously well and presented with sudden death. Autopsy showed nodules of sarcoid granuloma involving the heart, lungs and lymph nodes. Case two was a 47-year-old Indian lady who complained of reduced effort tolerance. Echocardiography showed that she had restrictive hypertrophic cardiomyopathy with heart failure. Seven months after initial presentation, she developed worsening of heart failure and died. Autopsy revealed involvement of the heart, lungs and liver by sarcoidosis.
The authors describe the case of a 50-year-old man with chronic progressive external ophthalmoplegia (CPEO), diabetes mellitus (DM), and coronary artery disease. The patient had no cardiac conduction abnormalities. During coronary artery bypass surgery, his heart and two skeletal muscles were biopsied. All three muscles showed ragged red fibers. The heart muscle showed significant glycogen accumulation. Analysis of mitochondrial DNA (mtDNA) showed a 5019-base-pair deletion, with no duplications. There were morphologically abnormal mitochondria in all 3 muscles, with clinically apparent difference in preservation of function. The combination of diabetes mellitus and mtDNA deletion is fortuitous, as they can be causally linked. The cardiac pathology allows speculation about the possible adaptive processes that may occur in the heart in DM. There are few reported cases with CPEO and excess glycogen in the heart. Most show deposition of fat and poorer clinical outcomes as compared to those with glycogen deposition. This observation may lend support to the hypothesis that in the myocardium, adaptive responses are mediated via changes in glucose handling, whereas alterations in fat metabolism likely represent maladaptation.
This is a case report of 16-year-old adolescent school boy who died due to unusual calcification of coronary arteries. He died while cycling with his friends. While cycling fast he fell. He was brought dead to hospital. At times unsuspected cardiac lesions cause sudden death during extraneous physical activities in healthy persons. Sudden death in adolescents is not very common. It is an unusual case as apparently healthy adolescent boy actively participating in sports had stony hard coronary arteries. The coronaries showed advanced calcification and early bone formation. The myocardial septum had extensive fibrosis. The pathogenesis and other possible similar conditions are also discussed in the report.
Palm oil used worldwide contains considerable amounts of antioxidants, namely, vitamin E and carotenes. The purpose of the study was to observe the effect of heated palm oil on blood pressure and observe the cardiac histological changes in rats.
Giant cell myocarditis (GCM) is a rare but fatal disease of idiopathic origin. It results in focal necrosis of myocardium. This is a case report of middle aged Malaysian Indian female who died due to cardiac tamponade due to rupture myocardium and tear in the root of aorta. On naked eye examination, it simply resembled as recent as well as old fibrotic areas of myocardial infarction. She was clinically diagnosed as a case of obstructive cardiomyopathy with atrioventricular block, and was on pace maker. There was subendocardial fibrosis and left ventricular transmural infarction in the left ventricle. On histopathology, this was diagnosed as GCM, there were widespread areas of inflammatory cellular infiltration within the myocardium with multinucleated giant cells and granulomas interspersed with lymphocytes. Microscopic field showed up to 10 multinucleated giant cells. In this case, there were focal areas at multiple locations and caused uneven thickness in the left ventricle wall. Idiopathic GCM is very rare and causation of hemopericardium is the unique feature of this case. In this case the direct link of GCM with aortitis and rupture of left ventricle wall resulting in hemopericardium is shown. This case is documented through macroscopic as well as microscopic photographs in H&E, Ziel-Nelson, and GMS staining.
Series of experiments have been completed with Methamphetamine (MA). Some were with the higher, medium or lower duration of MA administration and some were with acute or chronic doses. Whatever may be the dose or duration the ultimate result came out with the further establishment of cardio-toxic effect of this drug. Cardiovascular symptoms related to MA toxicity include chest pain, palpitations, dyspnoea, hypertension, tachycardia, atrial and ventricular arrhythmias, and myocardial ischemia. MA abusers often go through a repeated pattern of frequent drug administrations followed by a period of abstinence. Previous studies have focused largely upon the chronic effect of MA intake to major organs, such as the brains and the heart, by using animal experiments. However, there is a lack of research into the effects of acute dose of MA, especially pertaining to the heart. To clarify the effect of MA on myocardium, 22 male Wister rats aged six weeks were divided into MA, Placebo (P) and Control (C) group were examined following single intraperitoneal administration of MA at a dose of 50 mg/kg body weight. Normal saline was similarly injected in P group. Light microscopic changes was seen in the myocardium of MA treated group including cellular infiltration, with clusters of macrophage-like cells having large nuclei and little cytoplasm evident in the sub-endocardium region. There were presence of few macrophages, leucocytes, and spindle-like fibroblasts. Bringing in to account of cardiac changes by a single dose of MA, slogan should be voiced out to leave methamphetamine.