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PubMed1985

Vascular calcification in types II and IV hyperlipoproteinemia: radiographic appearance and clinical significance.

Nearly 90% of patients with clear-cut hyperlipidemia seen in clinical practice have type II or IV hyperlipoproteinemia. Previous studies have shown that these syndromes have different distributions of coronary artery atherosclerosis and different outcomes after coronary bypass grafting. A characteristic pattern of vascular calcification on chest films might have some prognostic value. Therefore, to determine the location and extent of aortic root and coronary artery calcification seen on chest films, 33 consecutive patients with type II and 17 with type IV hyperlipoproteinemia were studied who were admitted for coronary arteriography between 1970 and 1982. Among the 33 patients with type II disease, 21 women and 12 men, 22 had radiographically visible calcification that was different in distribution from that usually found in atherosclerotic disease. The ascending aorta was involved in 21 and the arch in 12. In eight patients, the calcium outlined a distinctive narrowing of the ascending aorta. Six patients had significant left ventricular obstruction; in five it was from aortic valve stenosis. Of the 17 type IV patients, 16 men and one woman, none had aortic calcification or left ventricular outflow obstruction, and only one had coronary artery calcification. These data demonstrate that patients with type II hyperlipoproteinemia have severe calcific atherosclerosis of the aortic root that often is visible on chest films. Such calcification may alert physicians to the presence of type II hyperlipoproteinemia and the high probability of severe coronary artery disease.

Adolescent↗
PubMed2000

[Efficacy of continuous intravenous drip infusion of disopyramide in hypertrophic obstructive cardiomyopathy during cardiogenic shock: a case report].

A 54-year-old woman was admitted to our hospital complaining of dyspnea due to hypertrophic obstructive cardiomyopathy. On admission, she was treated with 4 antiarrhythmic drugs and 2 beta-blockers. After 4 of these 6 drugs were withdrawn, the left ventricular outflow pressure gradient markedly increased and then she fell into cardiogenic shock. Therefore, disopyramide(600 mg/day) was administered by continuous intravenous drip infusion to reduce the left ventricular outflow pressure gradient. After intravenous administration of disopyramide, the left ventricular outflow pressure gradient markedly decreased from 100 to 16 mmHg and the cardiogenic shock could be improved. Continuous intravenous drip infusion of disopyramide is effective for the treatment of cardiogenic shock due to severe left ventricular outflow obstruction in patients with hypertrophic obstructive cardiomyopathy.

Anti-Arrhythmia Agents↗
PubMed1990

[Paradoxical left ventricular blood flow during the isovolumic relaxation period in non-obstructive hypertrophic cardiomyopathy: Doppler and M-mode echocardiographic study].

The left ventricular blood flow pattern during the isovolumic relaxation period was investigated in 17 patients with apical hypertrophy (mean 54 +/- 8 years) and 30 with asymmetric septal hypertrophy without left ventricular outflow obstruction (mean 54 +/- 14 years). Thirty-five age-matched normal subjects served as controls (mean 51 +/- 10 years). All cases were examined by pulsed Doppler echocardiography simultaneously with phonocardiography. In all the control subjects, an apically-directed flow was observed, which occurred simultaneously with the onset of the second heart sound. In contrast, a basally-directed flow was detected during the isovolumic relaxation period in 13 patients (76%) with apical hypertrophy and in 28 (93%) with asymmetric septal hypertrophy. In these cases, an apically-directed flow was often observed before the second heart sound. Standard M-mode echocardiography revealed a significant increase in the left ventricular short-axis dimension at the base during the isovolumic period in patients with hypertrophic cardiomyopathy, while the normal controls showed no significant change. Moreover, peak velocity of the basally-directed flow correlated significantly with the rapidity of dilatation of the basal dimension (r = 0.61, p less than 0.01). Thus, this basally-directed blood flow in the left ventricle during the isovolumic relaxation period may be caused by the asynchronous left ventricular dilatation during the isovolumic period.

Adult↗
PubMed2000

Dual-chamber pacing in hypertrophic cardiomyopathy.

This review focuses on recent developments in the field of pacing in hypertrophic cardiomyopathy (HCM). Regarding mechanisms of action, recent data indicates that pacing acts by inducing dysynchronous left ventricular activation, thus reducing contractility and increasing end-systolic volume. Following several positive uncontrolled studies, three randomized crossover trials, with a total of approximately 140 patients, have now confirmed that gradients are on average halved with pacing but the reduction in symptoms has been modest and maximum exercise capacity has not been improved. These studies have identified a placebo effect from pacemaker implantation in HCM and have questioned the efficacy of pacing as a symptomatic therapy for HCM. There is probably a subgroup of patients with HCM who respond to permanent dual-chamber pacing but their precise identification is not yet clear. Permanent pacing should continue to be considered as one option in the management of the patient with drug refractory, symptomatic obstructive HCM.

Cardiac Pacing, Artificial↗
PubMed1985

Cardiomyopathies and their role in sudden death.

Frequent ventricular premature complexes, complex ventricular ectopic activity and asymptomatic ventricular tachycardia are common to both hypertrophic and dilated cardiomyopathy; in both conditions, sudden death is a common occurrence. Asymptomatic young patients with hypertrophic cardiomyopathy who have a family history and a high incidence of ventricular arrhythmias have a particularly high incidence of sudden death. In patients with hypertrophic cardiomyopathy, efforts to attribute sudden death to the cardiac index, left ventricular end-diastolic pressure, left ventricular outflow obstruction, ejection fraction, age, symptomatic state and septal thickness have been unrewarding. Myocardial hypertrophy and disordered myocardial cell arrangement are the likely substrates for the development of ventricular arrhythmias in hypertrophic cardiomyopathy. Ventricular fibrillation preceded by ventricular tachycardia appears to be the terminal event in most patients who die suddenly. In some patients, cardiac asystole is the terminal event. Additional factors playing a role in the development of the substrate for sudden death in patients with hypertrophic cardiomyopathy vary in importance on an individual basis. These factors include narrowing of septal arteries and the artery to the atrioventricular node, preservation of fetal anatomy with dispersion in the atrioventricular node and His bundle, fibrosis of the sinus node, clefts in the septum, multiple atrioventricular pathways and massive myocardial infarction. Patients with dilated cardiomyopathy appear to have the highest incidence of ventricular arrhythmias of any disease yet studied. The substrate for the development of ventricular arrhythmias in these patients appears to be myocardial hypertrophy and myocardial fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1999

Clinical profile of hypertrophic cardiomyopathy identified de novo in rural communities.

OBJECTIVES: The purpose of this study was to assess the extent to which hypertrophic cardiomyopathy (HCM) exists unsuspected and undetected in the general population. BACKGROUND: Hypertrophic cardiomyopathy is a disease with diverse natural history for which the potential to produce adverse consequences has been emphasized. However, the possibility of this disease remaining clinically dormant for many years has not been as widely appreciated. Certainly, the clinical recognition of previously undiagnosed patients with HCM may be advantageous by permitting risk stratification for sudden cardiac death or for timely pharmacologic therapy when symptoms intervene. METHODS: We prospectively conducted an echocardiographic survey in 64 primarily rural communities within Minnesota (populations < 10,000) over a 33-month period. RESULTS: A total of 15,137 echocardiograms were performed at the request of primary care physicians for the purpose of excluding cardiovascular abnormalities. Hypertrophic cardiomyopathy was identified in 44 patients during the survey (0.29%), and 29 of these patients (0.19% of the 15,137 echocardiograms) had not been previously identified as having cardiac disease or HCM. At diagnosis, ages were 16 to 87 years (mean 57); 14 patients were > or = 60 years of age, and only two were < 30 years. Twenty-four patients (83%) had either no or only mild or transient symptoms; 5 (17%) evidenced severe functional limitation; in eight patients the onset of symptoms had been deferred until > or = 70 years of age. Basal left ventricular outflow obstruction (gradients 20 to 82 mm Hg) was evident in 11 patients (38%). Relatively mild phenotypic expression of the disease was substantiated by localized patterns of left ventricular wall thickening occurring more commonly than diffusely distributed hypertrophy (48% vs. 7%, respectively), and electrocardiograms that were frequently normal (about 25%) and rarely showed evidence of left ventricular hypertrophy (10%). CONCLUSIONS: These prospectively assembled data show that HCM may remain clinically dormant and undetected within community-based rural populations for many years (often to advanced ages) with a not inconsequential prevalence similar to that of HCM in the general population.

Adolescent↗
PubMed1998

[Aneurysm of the membranous ventricular septum with ventricular septal defect, mitral and tricuspid insufficiency].

A seventy-year-old man was admitted at our hospital because of dyspnea. Echocardiogram and left ventriculogram showed an aneurysm formation of the membranous ventricular septum and small left-to-right shunt through ventricular septum defect and also severe mitral and tricuspid insufficiency. Operation was performed after medical therapy for congestive heart failure. During operation, mitral leaflets showed no organic lesions nor prolapse, but the annulus was dilated. The cause of mitral insufficiency, we thought, might be congenital, and the annulus dilatation was caused of mitral insufficiency, we thought, might be congenital, and the annulus dilatation was caused to produce tricuspid insufficiency secondary. The ventricular septal communication became small (diameter; 5 mm) and was associated with aneurysm formation of the remaining portion of the membranous septum. And the aneurysm, protruding to the septal leaflet of tricuspid valves, enhanced tricuspid insufficiency. It was reported by many authors that the aneurysm formation was related to spontaneous closure of ventricular septal defect. Patients with small ventricular septal defect, without any symptoms, must be followed intensively, or they might get cardiac complications, such as arrhythmia, right ventricular outflow obstruction, tricuspid insufficiency, and so on.

Aged↗
PubMed1980

Cardiac tumours: non-invasive detection and assessment by gated cardiac blood pool radionuclide imaging.

Four patients with cardiac tumours were investigated by gated cardiac blood pool radionuclide imaging and echocardiography. Contrast angiocardiography was performed in three of the cases. Two left atrial tumours were detected by all three techniques. In one of these cases echocardiography alone showed additional mitral valve stenosis, but isotope imaging indicated tumour size more accurately. A large septal mass was detected by all three methods. In this patient echocardiography showed evidence of left ventricular outflow obstruction, confirmed at cardiac catheterisation, but gated isotope imaging provided a more detailed assessment of the abnormal cardiac anatomy. In the fourth case gated isotope imaging detected a large right ventricular tumour which had not been identified by echocardiography. Gated cardiac blood pool isotope imaging is a complementary technique to echocardiography for the non-invasive detection and assessment of cardiac tumours.

Adult↗
PubMed1983

Influence of aortic stenosis on the hemodynamic importance of coronary artery narrowing in dogs without left ventricular hypertrophy.

Coronary hemodynamic effects of controlled left ventricular outflow obstruction stimulating aortic valve stenosis were studied in 20 open-chest dogs, with and without graded coronary artery diameter narrowing. Aortic stenosis was regulated so that a mean left ventricular-aortic pressure gradient of 46 +/- 20 mm Hg (mean +/- standard deviation) was created as both heart rate and stroke volume were unchanged. In addition, during aortic stenosis, mean aortic pressure (105 +/- 17 to 84 +/- 15 mm Hg, p less than 0.05) and diastolic pressure time index/systolic pressure time index ratio (1.2 +/- 0.3 to 0.6 +/- 0.2, p less than 0.05) decreased and end-diastolic left ventricular pressure (7 +/- 4 to 14 +/- 6 mm Hg, p less than 0.05) increased. With no coronary narrowing, mean coronary flow increased during aortic stenosis (53 +/- 23 to 62 +/- 23 ml/min) as the percentage of diastolic flow increased (83 +/- 6 to 89 +/- 4) and endocardial/epicardial ratio decreased (1.14 +/- 0.16 to 0.95 +/- 0.24) (all p less than 0.05). Peak reactive hyperemic flow also decreased (168 +/- 85 to 125 +/- 73 ml/min, p less than 0.05). This value with no coronary narrowing was similar to peak hyperemic flow with 60% narrowing without aortic stenosis. With 90% coronary narrowing, mean coronary flow decreased with or without aortic stenosis. Transmural flow distribution also decreased but was lower during aortic stenosis (0.86 +/- 0.19 to 0.61 +/- 0.25, respectively; p less than 0.05). These data suggest that although mean coronary flow is increased during aortic stenosis, endocardial flow may be limited, and coronary reserve exposed during reactive hyperemia appears decreased. When a coronary artery is narrowed, aortic stenosis has an even more important hemodynamic influence on the coronary circulation.

Acute Disease↗
PubMed1997

Potential role of mechanical stress in the etiology of pediatric heart disease: septal shear stress in subaortic stenosis.

OBJECTIVES: The objective of this study was to show elevations in septal shear stress in response to morphologic abnormalities that have been associated with discrete subaortic stenosis (SAS) in children. Combined with the published data, this critical connection supports a four-stage etiology of SAS that is advanced in this report. BACKGROUND: Subaortic stenosis constitutes up to 20% of left ventricular outflow obstruction in children and frequently requires surgical removal, and the lesions may reappear unpredictably after the operation. The etiology of SAS is unknown. This study proposes a four-stage etiology for SAS that I) combines morphologic abnormalities, II) elevation of septal shear stress, III) genetic predisposition and IV) cellular proliferation in response to shear stress. METHODS: Morphologic structures of a left ventricular outflow tract were modeled based on measurements in patients with and without SAS. Septal shear stress was studied in response to changes in aortoseptal angle (AoSA) (120 degrees to 150 degrees), outflow tract convergence angle (45 degrees, 22.5 degrees and 0 degree), presence/location of a ventricular septal defect (VSD) (3-mm VSD; 2 and 6 mm from annulus) and shunt velocity (3 and 5 m/s). RESULTS: Variations in AoSA produced marked elevations in septal shear stress (from 103 dynes/cm2 for 150 degrees angle to 150 dynes/cm2 for 120 degrees angle for baseline conditions). This effect was not dependent on the convergence angle in the outflow tract (150 to 132 dynes/cm2 over full range of angles including extreme case of 0 degree). A VSD enhanced this effect (150 to 220 dynes/cm2 at steep angle of 120 degrees and 3 m/s shunt velocity), consistent with the high incidence of VSDs in patients with SAS. The position of the VSD was also important, with a reduction of the distance between the VSD and the aortic annulus causing further increases in septal shear stress (220 and 266 dynes/cm2 for distances of 6 and 2 mm from the annulus, respectively). CONCLUSIONS: Small changes in AoSA produce important changes in septal shear stress. The levels of stress increase are consistent with cellular flow studies showing stimulation of growth factors and cellular proliferation. Steepened AoSA may be a risk factor for the development of SAS. Evidence exists for all four stages of the proposed etiology of SAS.

Adolescent↗
PubMed1992

Transcriptional regulation of left ventricular beta-adrenergic receptors during chronic hypoxia.

beta-Adrenergic receptor downregulation is the end result of cellular adaptation to prolonged agonist exposure. The factors mediating receptor downregulation include receptor phosphorylation, receptor movement from the plasma membrane to intracellular sites, and alterations in nascent receptor synthesis. We have previously demonstrated a downregulation of the left ventricular beta-receptor during chronic hypoxia in vivo. To determine the mechanism of this downregulation, we produced chronic hypoxia in seven newborn lambs by creating right ventricular outflow obstruction and an atrial septal defect. Oxygen saturation was reduced to 65-74% for 2 weeks. Six lambs served as normoxic controls. Sarcolemmal membrane and cytosolic fractions were prepared from left ventricular free wall samples. beta-Receptor density in each fraction was determined with the radioligand [125I]iodocyanopindolol. Steady-state levels of beta-receptor mRNA were determined by Northern blot analysis using a beta 1-adrenergic receptor cDNA probe. During chronic hypoxia, left ventricular membrane beta-adrenergic receptor density decreased by 55% (153 +/- 28 fmol/mg for hypoxic lambs versus 342 +/- 79 fmol/mg for control lambs, p < 0.05). There was no corresponding increase in beta-receptor density in the cytosolic fraction (23 +/- 3 fmol/mg for hypoxic lambs versus 33 +/- 9 fmol/mg for control lambs, p = NS), nor was there a significant change in the ratio of beta 1-receptor/beta 2-receptor subtypes as assessed by radioligand binding (beta 1 subtype, 84.1 +/- 10.1% for hypoxic lambs versus 93.2 +/- 8.8% for control lambs; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Coarctation of the aorta in the syndrome of absent pulmonary valve with ventricular septal defect.

The case of a male child is reported in which the syndrome of absent pulmonary valve and ventricular septal defect was associated with anomalous drainage of the right superior pulmonary vein into the superior vena cava, atrial septal defect, a right aortic arch, and an aortic isthmic coarctation. The combination of aortic coarctation with a high degree of right-ventricular outflow obstruction has not been reported so far in the literature. This case shows that there is no proof of aplasia of the ductus arteriosus in the syndrome of absent pulmonary valve and ventricular septal defect. Most likely, there is an early involution of the ductus arteriosus; persistence of the ductus arteriosus would not be compatible with fetal survival.

Abnormalities, Multiple↗
PubMed1990

[Transaortic myectomy for hypertrophic obstructive cardiomyopathy--efficacy of intraoperative pressure measurement].

The many aspects of postoperative course of hypertrophic obstructive cardiomyopathy (HOCM) have been apparent, while many studies concerning long-term follow up have been published in recent years. Many surgical approaches have been performed but recently transaortic subvalvular myectomy is most common. This study reviews 22 patients with HOCM operated on between 1984 and 1989. Transaortic approach was used for all adult patients. One patient had a complication with an iatrogenic VSD, which was closed by Dacron patch during the procedure. There was one hospital death; She is a 67 year-old woman who died due to an acute abdomen. All 14 patients followed up over 3 months had significant functional improvement. Our retrospective study suggests that myectomy in patient with HOCM seems to be not only palliative but curative operative method. Left atrial- and left ventricular dimension tended to normalize in the postoperative course. The intraoperative estimation of Brockenbrough phenomenon is effective to assess the release of left ventricular outflow obstruction.

Adult↗
PubMed1995

Tetralogy of Fallot: prenatal diagnosis and postnatal survival.

OBJECTIVES: To correlate prenatal echocardiographic findings with infant outcome in a large screening population affected by tetralogy of Fallot. METHODS: Inclusion criteria required confirmed postnatal cardiac diagnosis, at least one fetal ultrasound examination with satisfactory heart visualization, and infant delivery at our institution. Aortic and pulmonary artery diameters were measured from real-time ultrasound or videotaped scans and compared against published nomograms. The pulmonary artery to aorta ratio was also evaluated in a similar manner. Infant survival was assessed 1 year after delivery. RESULTS: Seventeen fetuses were confirmed to have a ventricular septal defect and an overriding aorta with varying degrees of right ventricular outflow obstruction after delivery. All karyotypes were normal. Ultrasound screening identified 12 of 17 abnormal hearts at a mean gestational age of 22.9 +/- 5.1 weeks; two of these fetuses were thought to have only ventricular septal defect before delivery. Five fetuses had enlarged aortic roots during the initial scan. Only two of the ten fetuses with a measurable pulmonary artery had initial sonographic evidence for valve stenosis. Six other pulmonary arteries became abnormally small with advancing pregnancy. The pulmonary artery to aorta ratio was decreased in six of the ten fetuses with a measurable pulmonary artery. Sixteen infants survived at least 1 year after birth and successfully completed either corrective or palliative cardiac surgery. CONCLUSION: Fetuses with tetralogy of Fallot may present with only a ventricular septal defect and aortic septal override by prenatal ultrasound examination. Pulmonary artery stenosis is not always present at initial ultrasound examination, but this finding can develop or worsen during pregnancy. Furthermore, a normal aortic diameter does not exclude tetralogy of Fallot. Infant survival appears to be favorable in the absence of other major structural or chromosomal anomalies.

Female↗
PubMedDate not supplied

Pathology of the heart and conduction system in a case of sudden death due to a cardiac fibroma in a 6-month-old child.

A 6-month-old female infant considered to be in good health died suddenly and unexpectedly. Post-mortem examination was requested, with clinical diagnosis of sudden infant death syndrome. Gross examination revealed, however, the presence of a cardiac mass 4.5 X 4 x 3.5 cm in diameter. Histological examination of the heart confirmed the presence of a cardiac fibroma. In the present case, the sudden death could have been due to the left ventricular outflow obstruction, as much as to conductive disturbances caused by overstretching and compression of the atrioventricular node and of the bundle branches. Hemodynamic and conductive abnormalities are presumed to have provoked bradycardia degenerating into ventricular fibrillation and sudden death. Necroscopy studies of sudden death should always include histological examination of the cardiac conduction system but seldom do.

Female↗
PubMed1996

[Doppler echocardiographic investigation of cardiomyopathies].

There are three types of cardiomyopathy: hypertrophic, dilated and restrictive. The diagnosis and prognosis of these three types may be assessed from Doppler echocardiographic data. In hypertrophic cardiomyopathy, the diagnostic criterion is parietal hypertrophy. This hypertrophy is asymmetrical and usually affects the interventricular septum. Ventricular outflow obstruction is not necessarily present. The left ventricle is small and analysis of mitral inflow usually shows abnormal relaxation (E/A ratio < 1). The prognosis of this type of cardiomyopathy seems to be related to ventricular arrhythmias and the relationship between the hypertrophy and the presence of arrhythmias remains controversial. Dilated cardiomyopathy is characterized by ventricular walls of normal or decreased thickness, an increase in left ventricular dimensions and a reduction in the ejection fraction. An end-diastolic left ventricular dimension > 70 mm and an ejection fraction < 25% are poor prognostic factors. Left ventricular filling is abnormal and severe cases show a restrictive type of profile; in this case, an E/A ratio > 2 carries a poor prognostic. A mitral deceleration time of E wave < 150 msec usually indicates a bad outcome. Restrictive types of cardiomyopathy are more rare, amyloidosis being the commonest cause. Symmetrical wall thickening and a small ventricular chamber are observed. In advanced stages with abnormal systolic function, an E/A mitral ratio > 2 and deceleration time < 150 msec, the outcome is rapidly fatal.

Adult↗