1/15. An unusual case of ST elevation in a 39-year-old man.A 39-year-old man presented to a university hospital emergency department with anginal chest pain, ventricular tachycardia and ST elevation in the anterolateral leads (V3 to V6, I and aVL). Due to discrepancies in the history and physical examination, thrombolysis was withheld until a past electrocardiogram could be obtained, which was unchanged. Subsequent investigations revealed no evidence of myocardial necrosis, and the patient was diagnosed with hypertrophic cardiomyopathy. This is the first reported case of hypertrophic cardiomyopathy with ST elevation as the predominant electrocardiographic abnormality. In patients with discrepancies in the clinical presentation, it is essential to obtain past elecrocardiograms to ensure appropriate utility of thrombolysis.- - - - - - - - - - ranking = 1keywords = physical examination, physical (Clic here for more details about this article) |
2/15. Proximal trisomy of 1q mosaicism in a girl with hypertrophic cardiomyopathy associated with wolff-parkinson-white syndrome and multiple congenital anomalies.We report an African American female who is mosaic for partial trisomy of 1q due to a direct duplication of 1q12 to 1q25. The child has hypertrophic cardiomyopathy with wolff-parkinson-white syndrome. The physical features include micrognathia, cleft palate, low set ears, posteriorly placed thumbs, and syndactyly of the second and third toes of both feet. Other abnormalities include intestinal malrotation, scoliosis, mental retardation, cerebral palsy, and hydrocephalus. There was also a selective deficiency of antibody responses to polysaccharide antigens. Proximal duplication of chromosome 1q is rare and has not been previously associated with hypertrophic cardiomyopathy. Most known gene disorders related to hypertrophic cardiomyopathy are autosomal dominant missense mutations in sarcomeric protein genes; however, none of the sarcomeric genes previously linked to hypertrophic cardiomyopathy are in this region. This finding thus highlights the possibility of additional genetic mechanisms for hypertrophic cardiomyopathy.- - - - - - - - - - ranking = 0.18253012565236keywords = physical (Clic here for more details about this article) |
3/15. Hypertrophic cardiomyopathy complicated by severe bradycardias: a pedigree report.We describe four patients with nonobstructive hypertrophic cardiomyopathy (HCM) from an extended Chinese family. The patients had remarkably similar physical and echocardiographic findings including a harsh localized systolic murmur and apical left ventricular hypertrophy. All four had severe sinus bradycardia and atrial-ventricular conduction block (AVB) manifest by recurrent syncope. Two died suddenly due to bradycardia. Holter monitoring showed no tachycardias. Late potentials were not present. We conclude that this unusual form of HCM may be caused by a new and as yet unknown gene mutation.- - - - - - - - - - ranking = 0.18253012565236keywords = physical (Clic here for more details about this article) |
4/15. Hypercontractile cardiac states simulating hypertrophic cardiomyopathy.Hypertrophic cardiomyopathy (HCM) or idiopathic hypertrophic subaortic stenosis (IHSS) has been defined as an autosomal dominant myocardial disease characterized by specific physical findings, echocardiographic features, asymmetric septal hypertrophy and disordered myocardial architecture. Echocardiographic and scintiphotographic studies failed to reveal evidence of asymmetric septal hypertrophy in four patients with systolic anterior movement of the mitral valve and the typical ausculatory and peripheral pulse abnormalities characteristic of HCM. Postmortem examimination in one patient demonstrated mild concentric left ventricular hypertrophy and a normal arrangement of myocardial muscle fibers. These observations in four patients demonstrate that both systolic anterior movement of the mitral valve and the physical findings characteristic of HCM are not specific for the autosomal dominant myocardial disease characterized by asymmetric septal hypertrophy and abnormal septal histology.- - - - - - - - - - ranking = 0.36506025130472keywords = physical (Clic here for more details about this article) |
5/15. Hypertrophic cardiomyopathy in a college athlete.The greatest catastrophy in sports is an athlete's unexpected sudden death. Identifying those athletes at risk remains a great challenge to physicians performing preseason examinations. Hypertrophic cardiomyopathy is the most common cause of nontraumatic sudden death in athletes. Most cases of this diseased heart are diagnosed easily by echocardiography. The case presented exemplifies the attention to detail required to differentiate the borderline diseased heart from the conditioned athletic heart. Once a diagnosis of hypertrophic cardiomyopathy is made, further participation in intense physical exercise is discouraged. This recommendation is necessary despite the unknown relative sudden death risk for the minimal criteria cases.- - - - - - - - - - ranking = 0.18253012565236keywords = physical (Clic here for more details about this article) |
6/15. Woolly hair and palmoplantar hyperkeratosis may present with hypertrophic cardiomyopathy.Woolly hair and palmoplantar hyperkeratosis is an infrequent autosomal recessive ectodermal disorder that may be associated with arrhythmogenic right ventricular dysplasia (Naxos disease) or dilated cardiomyopathy. We report the sporadic occurrence of the aforementioned skin-hair anomalies in a patient with physical findings compatible with Noonan's syndrome and hypertrophic cardiomyopathy-an association heretofore not described.- - - - - - - - - - ranking = 0.18253012565236keywords = physical (Clic here for more details about this article) |
7/15. Tako-Tsubo cardiomyopathy: new insights into the possible underlying pathophysiology.Tako-Tsubo cardiomyopathy is characterised by an atypical distribution of left ventricular (LV) dysynergy with apical ballooning and compensatory basal hyperkinesis. coronary angiography is normal. Several substrates have been put forward to explain the underlying pathophysiology such as raised catecholamine levels (due to physical or emotional stress), multivessel epicardial coronary spasm or diffuse microvascular spasm. However, the pathophysiology has not yet been fully clarified. We present a series of cases whose findings could explain the mechanism underlying this syndrome. Four consecutives patients, all female, were admitted with the clinical features typical of Tako-Tsubo syndrome. In all, severe widespread transient LV mid-apical a/dyskinesia was associated with a mid-cavity dynamic obstruction which resolved prior to the resolution of the LV wall motion abnormalities. In all cases the dynamic LV obstruction was related to localised mid-ventricular septal thickening. After improvement in wall motion, a low-dose strain/strain rate dobutamine stress-echocardiography (DSE) was performed to determine the underlying ischaemic substrate. This provoked an LV mid-cavity gradient at peak dose in all. Regional deformation changes during DSE showed the affected myocardium to have the typical response diagnostic of regional stunning. CONCLUSION: We postulate that an important unrecognised factor in the development of Tako-Tsubo cardiomyopathy is the presence of abnormal myocardial functional architecture (such as localised mid-ventricular septal thickening), which in the presence of dehydration and/or raised catecholamine levels due to physical or emotional stress, leads the development of a severe transient LV mid-cavity obstruction. This effectively sub-divides the LV into two functionally different chambers with a marked increase in wall stress in the high pressure distal apical chamber. This, in combination with the abnormal high circulating catecholamine levels, induces widespread sub-endocardial ischaemia which is unrelated to a specific coronary artery territory. With rehydration/fall in catecholamine levels the interventricular gradient resolves and distal function recovers. Low dose SR/S DSE confirms that the distal ischaemic substrate is myocardial stunning.- - - - - - - - - - ranking = 0.36506025130472keywords = physical (Clic here for more details about this article) |
8/15. Eosinophilic heart disease presenting with features suggesting hypertrophic obstructive cardiomyopathy.We report a 25-year-old female with characteristic features of eosinophilic heart disease on clinical presentation, echocardiography, cardiac catheterization, and LV endomyocardial biopsy. Concomitant physical examination and echocardiographic findings suggesting hypertrophic obstructive cardiomyopathy resolved during treatment with anticoagulation and prednisone therapy.- - - - - - - - - - ranking = 1keywords = physical examination, physical (Clic here for more details about this article) |
9/15. A long-term follow-up study of acute myocarditis an electrocardiographic and echocardiographic study.In an attempt to prove that myocarditis may be a cause of idiopathic cardiomyopathy, 10 cases with acute myocarditis were involved in a long-term follow-up study. There were 9 males and 1 female patient, ranging in age from 22 to 63 years. The etiology of myocarditis was idiopathic in 9 cases and rubella virus in 1 case. Clinical findings in the acute stage consisted of congestive heart failure in 6 cases, adams-stokes syndrome in 2 cases and cardiomegaly in 2 cases. The mean follow-up period was 55 months. follow-up studies included physical examinations, 12-lead ECG, chest x-rays and two-dimensional echocardiograms. Various patterns of residual ECG abnormalities in the chronic stage were found, such as conduction disturbance in 1 case, pseudoinfarction pattern in 4 cases, ST-T changes in 2 cases and premature ventricular contractions in 2 cases. The cardiothoracic ratio of all cases was 60 /- 4% in the acute stage. Two cases (Case 1 and 2) died 16 and 36 months after the acute onset, respectively. Four cases had residual cardiomegaly even in the last study period. An echocardiographic follow-up study of 7 cases disclosed progressive left ventricular (LV) dilatation and dysfunction in 3 cases, regression of LV dilatation in 2 cases and stable LV function in 2 cases. Two cases out of 3 with progressive LV dilatation and dysfunction expired after the acute illness. It was therefore suggested that acute myocarditis may cause LV dilatation and/or wall hypertrophy and that idiopathic cardiomyopathy may represent the end-stages of previous myocarditis.- - - - - - - - - - ranking = 1keywords = physical examination, physical (Clic here for more details about this article) |
10/15. Hypercontractile cardiac state mimicking hypertrophic subaortic stenosis.Idiopathic hypertrophic subaortic stenosis (IHSS) is a disease manifested as a spectrum of various clinical and laboratory findings. We present the case of a patient with classical clinical and hemodynamic findings of IHSS who lacked all of the typical echocardiographic features of the disease. The case emphasizes the need for diligent use of bedside physical examination and vasoactive manipulation of systolic murmurs whenever functional left ventricular outflow tract obstruction is suspected, since it can occasionally be missed by echocardiography.- - - - - - - - - - ranking = 1keywords = physical examination, physical (Clic here for more details about this article) |
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