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At least 19 recordsLinked to original sources
PubMed1983

Differential diagnosis of hypertrophic cardiomyopathies: typical (subaortic) hypertrophic obstructive cardiomyopathy, atypical (mid-ventricular) hypertrophic obstructive cardiomyopathy and hypertrophic non-obstructive cardiomyopathy.

Previous clinical studies in patients with hypertrophic cardiomyopathies predominantly comprised patients with typical subaortic HOCM and in many other studies patients with 'hypertrophic' cardiomyopathies were investigated; i.e. no distinction was made between patients with the typical obstructive, the atypical obstructive and the non-obstructive forms of hypertrophic cardiomyopathy. In addition, in the more differentiated studies, the differential diagnosis between HOCM and HNCM was based mainly on the presence and absence of the subaortic pressure gradient. This is also true for the clinical characterization of both types of hypertrophic cardiomyopathy. Finally, diagnostic descriptions of atypical (mid-ventricular) HOCM exist only in the form of case reports, i.e. they are not based on observations in a large number of patients. Therefore a comparative study in 353 patients with hypertrophic cardiomyopathies was designed to characterize the clinical picture of patients with HNCM and with atypical HOCM in relation to typical HOCM with special reference to the differential diagnosis. The study revealed a profoundly different diagnostic profile of the three subsets of hypertrophic cardiomyopathies. The distinction between the three subsets may serve as a more differentiated basis for clinical studies related to diagnosis, therapeutic approaches, long-term follow-up observations and prognostic evaluation of patients with hypertrophic cardiomyopathies.

Adolescent↗
PubMed2005

[Cardiomyopathies II. Hypertrophic cardiomyopathy, restrictive cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy].

This review focuses on hypertrophic (HCM), restrictive (RCM) and arrhythmogenic right ventricular cardiomyopathies (ARVC). The clinical phenotype of HCM depends not only on the gene mutations involved, but also on "modifier genes". It is characterized by an asymmetrical hypertrophy. Investigations of endomyocardial biopsies (EMBs) typically reveal a disarray of the hypertrophied cardiomyocytes. Percutaneous septum ablation has gained relevance as the treatment of choice in hypertrophic obstructive cardiomyopathy. Myocardial and endomyocardial RCM-forms can be differentiated. Enlargement of the atria in concert with normal dimensions of the ventricles and almost normal systolic contractility as well as the dip-plateau phenomenon are characteristic findings in RCM. EMB diagnostics are pivotal to identify the causes underlying secondary RCM types. Treatment is directed at heart failure and specifically at the underlying disease. With ARVC, apoptosis, viral infection/inflammation and genetic dystrophy result in fibrofatty degeneration primarily of the right, and with further progression also of the left ventricle. The primary treatment goal in ARVC is prevention of sudden cardiac death. As for other cardiomyopathies, there is increasing evidence for the superiority of ICD compared with pharmacological approaches.

Cardiomyopathies↗
PubMed1991

Beta-adrenergic blockade in dilated cardiomyopathy, ischemic cardiomyopathy, and other secondary cardiomyopathies.

Beta-blockers were initially given to patients with chronic heart failure due to ischemic heart disease and resting tachycardia. The prompt effect on severe backward heart failure was directly associated with an immediate fall in heart rate. This observation led to long-term administration to patients with idiopathic dilated cardiomyopathy and, later, to patients with ischemic cardiomyopathy and secondary cardiomyopathies as well. Due to marked down-regulation of beta receptors, patients with heart failure are extremely sensitive to beta blockade. A test dose of metoprolol 5 mg b.i.d. for 2 days is recommended to select patients for long-term beta-blockade, followed by careful titration with increment in dose over 6 weeks. One important effect of beta-blockade in the early phase of treatment is a reduction in the myocardial energy demand early after the onset of long-term treatment. After 1 month of treatment with beta-blockers, marked improvement of diastolic function is observed. This effect might be attributed to inhibition of calcium overload. After 3 months of treatment, an increase in ejection fraction can be observed, which might be attributed to upregulation of beta receptors. The withdrawal of long-term treatment was followed by a deterioration of heart function in 61% of patients and improvement was seen after reinstitution of beta-blockade. There was an increase in cardiac index and stroke work index at rest as well as during supine exercise. A marked fall in left ventricular filling pressure at rest and unchanged filling pressure during supine exercise was noted, while exercise capacity increased by 25%. A similar pattern was seen in patients with ischemic cardiomyopathies and other secondary cardiomyopathies. However, the increase in ejection fraction in the ischemic cardiomyopathy group was lower (0.06) compared to the groups with dilated cardiomyopathy and other secondary cardiomyopathies (0.18).

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Features of mildly dilated congestive cardiomyopathy compared with idiopathic restrictive cardiomyopathy and typical dilated cardiomyopathy.

Congestive cardiomyopathy was recognized in eight patients with only mildly dilated ventricles (an echocardiographic ventricular diastolic dimension index of less than 10% to 15% above the normal range) but with other features typical of end-stage congestive cardiomyopathy. Such patients with mildly dilated cardiomyopathy (MDCM) represented 5% of heart transplant recipients with cardiomyopathy, who were analyzed by us. The clinical, echocardiographic, and hemodynamic data, as well as the gross and microscopic pathologic findings of the hearts in this group were compared with similar data in five patients with idiopathic restrictive cardiomyopathy (IRCM) and 10 patients with typical dilated cardiomyopathy (DCM). Compared with IRCM and DCM, patients with MDCM had a higher incidence of familial cardiomyopathy (p less than 0.009). The echocardiographic features of patients with MDCM and DCM were virtually identical, showing globular hearts with predominant left ventricular dilation and diffuse poor left ventricular contraction. Patients with IRCM had marked atrial dilation but less abnormality of left ventricular size and contraction parameters. On the basis of echocardiographic data, patients with IRCM and MDCM could be well segregated. Cardiac index and light microscopic examinations were similar in the three groups. However, electron microscopy showed a lack of myofibrillar loss in patients with IRCM, little or no myofibrillar loss in those with MDCM, and almost total myofibrillar loss in those with DCM. Patients with MDCM have a high prevalence of familial cardiomyopathy. Absolute heart size and electron microscopic features of the MDCM group were intermediate between IRCM and DCM, but other clinical, echocardiographic and hemodynamic findings were similar to typical DCM.

Adolescent↗
PubMed2005

[Cardiomyopathies. I: classification of cardiomyopathies--dilated cardiomyopathy].

Cardiomyopathies are common causes of heart failure and sudden cardiac death. According to the WHO classification, "specific" cardiomyopathies are differentiated from "idiopathic" cardiomyopathies. Thus, this classification is primarily based on pathophysiological characteristics. The diagnostic spectrum in cardiomyopathies comprises the entire spectrum of non-invasive and invasive cardiological examination techniques. The exact verification of certain cardiomyopathies necessitates additionally investigations. For example, immunohistological and molecular biological investigations of endomyocardial biopsies may confirm inflammatory cardiomyopathy, which is often induced by viruses. Several studies have shown that specific immunomodulatory treatment options can halt the progressive course of the disease. Several gene mutations have been identified in genetic/familial dilated cardiomyopathy. First-degree relatives should be screened for early stages. Primary prevention of sudden cardiac death shows increasing superiority of the implantable defibrillator compared with pharmacological approaches (i.e. amiodarone).

Cardiomyopathies↗
PubMed1998

Comparison of clinical and morphologic cardiac findings in patients having cardiac transplantation for ischemic cardiomyopathy, idiopathic dilated cardiomyopathy, and dilated hypertrophic cardiomyopathy.

This article compares intergroup and intragroup clinical and morphologic findings in patients with ischemic cardiomyopathy (IC), idiopathic dilated cardiomyopathy (IDC), and dilated hypertrophic cardiomyopathy (HC) undergoing cardiac transplantation (CT). Few previous publications have described findings in native hearts explanted at the time of CT. The explanted heart in 92 patients having CT was examined in uniform manner with particular attention to the sizes of the ventricular cavities and the presence of and extent of ventricular scarring. Of the 92 hearts examined, 47 had IC, 35 had IDC, and 10 had dilated HC. Although considerable degrees of intragroup variation occurred, the mean degree of left ventricular dilatation was similar among the patients with IC, IDC, and dilated HC. All patients with IC had left ventricular free wall scarring more extensive than that involving the ventricular septum, but the intragroup variation in the amounts of scarring was considerable. Nine of the 10 patients with dilated HC also had ventricular wall scarring, but it was more extensive in the ventricular septum than in the left ventricular free wall and involvement of the right ventricular wall also was present. Eight (23%) of the 35 IDC patients also had grossly visible ventricular scars but they were small and only 1 of the 8 had coronary narrowing and that was not in the distribution of the scarring. Narrowing of 1 or more epicardial coronary arteries >75% in cross-sectional area by plaque was present in all 47 IC patients, in 8 of the 35 IDC patients (7 had no ventricular scars), and in none of the 10 dilated HC patients. Coronary angiography was the major clinical tool allowing separation of the IC, IDC, and HC patients. Coronary angiography did not detect narrowing in any of the 8 patients with IDC who were found to have coronary narrowing on anatomic study. Thus, among patients with IC, IDC, and dilated HC having CT, distinctive anatomic features allow separation of patients with IC, IDC, and dilated HC, but within each group considerable variation in left ventricular cavity size and extent of ventricular scarring occurs.

Adult↗
PubMed2003

Hypertrophic cardiomyopathy: two homozygous cases with "typical" hypertrophic cardiomyopathy and three new mutations in cases with progression to dilated cardiomyopathy.

About 10% of cases of hypertrophic cardiomyopathy (HCM) evolve into dilated cardiomyopathy (DCM) with unknown causes. We studied 11 unrelated patients (pts) with HCM who progressed to DCM (group A) and 11 who showed "typical" HCM (group B). Mutational analysis of the beta-myosin heavy chain (MYH7), myosin-binding protein C (MYBPC3), and cardiac troponin T (TNNT2) genes demonstrated eight mutations affecting MYH7 or MYBPC3 gene, five of which were new mutations. In group A-pts, the first new mutation occurred in the myosin head-rod junction and the second occurred in the light chain-binding site. The third new mutation leads to a MYBPC3 lacking titin and myosin binding sites. In group B, two pts with severe HCM carried two homozygous MYBPC3 mutations and one with moderate hypertrophy was a compound heterozygous for MYBPC3 gene. We identified five unreported mutations, potentially "malignant" defects as for the associated phenotypes, but no specific mutations of HCM/DCM.

Adult↗
PubMed2004

Evolution of dilated cardiomyopathy (DCM) from idiopathic hypertrophic cardiomyopathy (IHCM) vs. inflammatory dilated cardiomyopathy (DCMi): a rare case of sudden death in an 8-year-old boy.

In rare cases, the diagnosis of hypertrophic and dilated cardiomyopathy (DCM) in children was established postmortem. Our case report deals with the sudden and unexpected death of an 8-year-old boy. The postmortem examination revealed non-obstructive hypertrophy with irregular arrangement of muscular fibers, dilatation of the ventricles, endocardial fibrosis, microfocal vacuolization with enlarged hyperchromatic nuclei, and signs of inflammation with interstitial fibrosis. We present an evolution from idiopathic cardiomyopathy to DCM. To some extent, there were morphologic signs of an inflammatory process that first led us to suspect a specific inflammatory DCM.

Cardiomyopathy, Dilated↗
PubMed1998

[Detection of enteroviral RNA in endomyocardial biopsies in inflammatory cardiomyopathy and idiopathic dilated cardiomyopathy].

The role of enteroviral myocardial infection in the development of dilated cardiomyopathy could only be substantiated after the introduction of molecular biological techniques (polymerase chain reaction, in-situ hybridization) in virological diagnostics of dilated cardiomyopathy. By using histological and especially immunohistological techniques for the detection of myocardial inflammation in patients with the tentative clinical diagnosis of dilated cardiomyopathy, a differentiation between inflammatory cardiomyopathy and idiopathic dilated cardiomyopathy on the basis of the WHO classification 1995 (31) was made. Inflammatory cardiomyopathy is defined by myocarditis in association with cardiac dysfunction and is diagnosed by established histological and especially immunohistological techniques. The combination of histological, immunohistological, and molecularbiological techniques enabled a subgroup analysis of the incidence of enteroviral myocardial RNA in patients with inflammatory cardiomyopathy in comparison to patients with idiopathic dilated cardiomyopathy. The study involved a total of 75 patients with impaired left ventricular function (EF < 50%) and the tentative clinical diagnosis of dilated cardiomyopathy. Right ventricular endomyocardial biopsies were obtained from all patients for further clarification of the cause of left ventricular functional disorder. All biopsies were analyzed for the presence of acute and chronic inflammatory myocardial alterations by histological ("Dallas" criteria) and immunohistological techniques (lymphocytic infiltrates, MHC antigen expression). Furthermore, each biopsy was examined by reverse transcriptase polymerase chain reaction (RT-PCR) in combination with Southern blot hybridization for the presence of enteroviral RNA. Active myocarditis was excluded in all patients by histological examination according to the "Dallas" criteria. Using immunohistological techniques, 26/75 patients (35%) had evidence for chronic inflammatory myocardial alterations in the sense of lymphocytic infiltrates (> or = 2,0 CD3 T-lymphocytes/ visual field at 400 magnification (HPF); > or = 7 CD3 T-lymphocytes/mm2). These patients were diagnosed as having inflammatory cardiomyopathy. To differentiate between patients with and without myocardial inflammation, cases with focal cellular infiltration and an average cell number between 2.5 and 2.0 CD3 T-lymphocytes/HPF and an increased expression of additional immune markers, i.e., MHC antigens, were not addressed in the group of patients with inflammatory cardiomyopathy. This is in contrast to Kühl et al (19). Consequently these patients were classified as patients with idiopathic dilated cardiomyopathy. These criteria of diagnosing myocardial inflammation were based on published results (20, 23, 26, 27, 49) and on our own control group (n = 85) (19) in which mean CD3 T-lymphocyte count/HPF in normal myocardial tissue were 0.7 (range 0.0-1.4). In addition, a subgroup analysis was performed of patients with a CD3 T-lymphocyte count > or = 3 CD3 T-lymphocytes/HPF (> or + 11 CD3 T-lymphocytes/mm2). The other 49/75 patients without myocardial inflammation (< 2.0 CD3 T-lymphocytes /HPF) were diagnosed as having idiopathic dilated cardiomyopathy. In 27/75 patients (36%), RT-PCR in combination with Southern blot hybridization revealed enteroviral RNA in the endomyocardial biopsies. The detection rate of enteroviral RNA did not differ between inflammatory cardiomyopathy (8/26 (31%)) and idiopathic dilated cardiomyopathy (19/49 39%)). In the subgroups of patients with a CD3 T-lymphocyte cell count > or = 3 CD3 T-lymphocytes/HPF (> or = 11 CD3 T-lymphocytes/mm2) (mean 4.4 +/-2.1 CD3 T-lymphocytes/HPF), three of the ten patients were enteroviral RNA positive (30%). In summary, the introduction of histological and immunohistological techniques in the extended diagnostics of dilated cardiomyopathy enables a subgroup analysis of the incidence of enteroviral myocardial RNA in

Adult↗
PubMed2000

[Definition and classification of cardiomyopathies and specific cardiomyopathies].

The cardiomyopathies were previously defined as "heart muscle diseases of unknown cause" and were differentiated from specific heart muscle disease with known cause. With increasing understanding of etiology and pathogenesis, the difference between cardiomyopathy and specific heart muscle disease has become indistinct. Accordingly in 1995 WHO/ISFC task force, the definition and classification of cardiomyopathies were revised as cardiomyopathies are defined as disease of the myocardium associated with cardiac dysfunction. On the other hand, since the classification has become established clinical entities, the terminology is preserved as follows: dilated cardiomyopathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy. While arrhythmogenic right ventricular cardiomyopathy is additionally included. The term specific cardiomyopathies is used to describe heart diseases that are associated with specific cardiac or systemic disorders. These were previously defined as specific heart muscle diseases. They included ischemic cardiomyopathy, valvular cardiomyopathy, hypertensive cardiomyopathy, inflammatory cardiomyopathy, metabolic cardiomyopathy, general system disease, muscular dystrophies, sensitivity and toxic reactions and peripartal cardiomyopathy. The cardiomyopathies are therefore classified by the dominant pathophysiology or, if possible, by etiological/pathogenetic factors.

Cardiomyopathies↗
PubMed1987

Clinical significance of early diastolic time intervals for the differentiation of idiopathic dilative cardiomyopathy from ischemic cardiomyopathy.

In order to differentiate idiopathic dilative cardiomyopathy from ischemic cardiomyopathy noninvasively, systolic time intervals (STIs) and early diastolic time intervals were investigated in patients with idiopathic dilative cardiomyopathy (n = 11), patients with ischemic cardiomyopathy (n = 8), and normal controls (n = 17). Minimal left ventricular pressure and pulmonary capillary wedge pressure (PCWP) were also measured to clarify the relationship between early diastolic time intervals and early diastolic hemodynamics. Cardiac function estimated by STIs was markedly depressed both in idiopathic dilative cardiomyopathy and ischemic cardiomyopathy, and there was no difference between the two diseases. In early diastolic time intervals, IIA-O time (the interval from the aortic component of the second heart sound to the O point of apexcardiogram) was significantly prolonged both in idiopathic dilative cardiomyopathy (144 +/- 31 (SD); p less than 0.01) and ischemic cardiomyopathy (153 +/- 15; p less than 0.01) compared to normal controls (126 +/- 11). IIA-MVO time (the interval from IIA to the mitral valve opening) in idiopathic dilative cardiomyopathy (49 +/- 23) was significantly shorter than that in normal controls (70 +/- 8; p less than 0.05). On the contrary, IIA-MVO time in ischemic cardiomyopathy (126 +/- 11) was markedly prolonged compared with normal controls (p less than 0.01) and idiopathic dilative cardiomyopathy (p less than 0.01). MVO-O time was significantly prolonged in idiopathic dilative cardiomyopathy (94 +/- 18; p less than 0.01). However, it was conversely shortened in ischemic cardiomyopathy (25 +/- 15) compared with normal controls (54 +/- 7; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Differentiation between primary dilated cardiomyopathy and ischemic cardiomyopathy based on right ventricular performance.

The differentiation of primary dilated cardiomyopathy from ischemic cardiomyopathy, though important, is difficult clinically and may require coronary angiography or metabolic imaging. Both patient groups have severe left ventricular dysfunction and severe wall motion abnormality. This study examined the differences in right ventricular performance between the two groups. There were 90 patients with a left ventricular ejection fraction less than 30% who had coronary angiography and multigated radionuclide angiography (MUGA). Of these, 69 had ischemic cardiomyopathy and 21 had primary cardiomyopathy. The left ventricular ejection fraction was similar; 22 +/- 6% in ischemic cardiomyopathy and 21 +/- 6% in primary cardiomyopathy. However, the right ventricular ejection fraction was higher in ischemic cardiomyopathy (38 +/- 16% versus 29 +/- 12%, p less than 0.01). There were 59 patients with right ventricular ejection fraction greater than or equal to 30%, of whom 50 patients (85%) had ischemic cardiomyopathy. The left ventricular and right ventricular volumes were determined by a count-based method. The right ventricular end-diastolic volume/left ventricular end-diastolic volume ratio was 0.57 in ischemic cardiomyopathy and 1.07 in primary cardiomyopathy (p less than 0.05). Thus assessment of right ventricular function may help differentiate primary from ischemic cardiomyopathy; a preserved right ventricular performance is highly suggestive of ischemic cardiomyopathy.

Cardiac Catheterization↗
PubMed1991

High output failure in patients with peripartum cardiomyopathy: a comparative study with dilated cardiomyopathy.

Although few studies have reported on relatively preserved ventricular function in patient with peripartum cardiomyopathy, the condition is usually believed to have the typical low-output congestive hemodynamic pattern of the dilated congestive cardiomyopathies. Two groups of patients, 14 with peripartum cardiomyopathy and 12 with dilated congestive cardiomyopathy who were matched for gender and age, were studied. They had normal blood pressure and similar New York Heart Association functional class, nutritional status, thyroid function and routine laboratory evaluation. All patients were catheterized during stable in-hospital compensation of heart failure, which was achieved by bed rest, sodium restriction, and administration of digoxin and diuretics long (more than 3 months) after delivery. Significant differences (p less than 0.05) between patients with peripartum cardiomyopathy and those with dilated congestive cardiomyopathy were observed in regard to: (1) cardiac index: 3.34 +/- 1.36 L/min/m2 versus 2.24 +/- 0.72 L/min/m2, (2) systemic vascular resistance: 1713 +/- 567 dynes.sec.cm-5 versus 2194 +/- 603 dynes.sec.cm-5, (3) right ventricular stroke work index: 8.6 +/- 4.2 g.M/m2 versus 14.8 +/- 8.2 g.M/m2 in the peripartum cardiomyopathy and the dilated congestive cardiomyopathy groups, respectively. Three of the patients with peripartum cardiomyopathy had resting cardiac index values that were even higher than the normal upper limit for our laboratory (4.5 L/min/m2): 4.80, 5.70, and 5.63 L/min/m2. They also had nearly normal left ventricular ejection fractions: 0.68, 0.41, and 0.51, respectively. These results indicate that, unlike the common dilated cardiomyopathy, the hemodynamic pattern in patients with peripartum cardiomyopathy is not homogeneous, and some patients have high-output failure and near normal left ventricular function.

Adult↗
PubMedDate not supplied

Upregulation of adhesion molecules and class I HLA in the myocardium of chronic chagasic cardiomyopathy and heart allograft rejection, but not in dilated cardiomyopathy.

The immunohistochemical expression of adhesion molecules and class I HLA in chronic chagasic cardiomyopathy were compared with heart allograft rejection and dilated cardiomyopathy, to obtain new knowledge on the occurrence of autoimmunity and inflammation in the pathogenesis of chronic chagasic cardiomyopathy. Semiquantitative immunohistochemistry was performed for CD8+ T cells, ICAM-1, VCAM-1, LFA-1, and class I HLA in frozen sections of myocardial biopsies from patients presenting chronic chagasic cardiomyopathy (group I, n = 12), heart allograft rejection (group II, n = 9) or dilated cardiomyopathy (group III, n = 9). A high mean number of CD8+ T cells/mm(2) was present in group I (18.26) and group II (28.60), but not in group III (0.83). The frequency of high expression for ICAM-1 and VCAM-1 on the endothelial and interstitial cells, and for class I HLA on the cardiomyocytes was greater in group I (100%, 33.3%, and 83.3%, respectively) and group II (100%, 66.7%, and 77.8%, respectively), compared to group III (66.7%, 0%, and 0%, respectively). ICAM-1 and VCAM-1 probably participate in the development of the lymphocytic inflammatory infiltrate present in chronic chagasic cardiomyopathy, as seen in heart allograft rejection. The overexpression of adhesion molecules and the induction of class I HLA on the cardiomyocytes are probably related to the high cytokine levels at the inflammatory sites in chronic chagasic cardiomyopathy. Although the induction of class I HLA on the cardiomyocytes is consistent with an autoimmune reaction, it should not be considered as irrefutable evidence for autoimmunity in chronic chagasic cardiomyopathy. The differential expression of adhesion molecules and class I HLA in dilated cardiomyopathy compared to chronic chagasic cardiomyopathy suggests differences in the pathogenesis of these cardiomyopathies.

Adult↗
PubMed2000

[Differential diagnosis of idiopathic cardiomyopathy from ischemic cardiomyopathy and hypertensive heart disease using non-invasive methods].

Although, the diagnosis of idiopathic cardiomyopathy is determined by cardiac catheterization including myocardial biopsy, non-invasive diagnosis is important. The most useful method is nuclear cardiology to differentiate dilated cardiomyopathy from ischemic cardiomyopathy. Cardiac images in ischemic cardiomyopathy have wider perfusion and metabolic defects than in dilated cardiomyopathy using Tl-201, Tc-99m perfusion tracers, I-123 BMIPP, N-13 NH3 and F-18 FDG. The degree of heterogenecity of the myocardium is higher in ischemic cardiomyopathy than in dilated cardiomyopathy by these tracers. Left ventricular hypertrophy is common finding in hypertension and hypertrophic cardiomyopathy. However, in hypertensive heart disease the left ventricular wall thickness rarely exceed than 20 mm, and the septal wall thickness/posterior wall thickness is not more than 1.5, which are frequently shown in hypertrophic cardiomyopathy. Right ventricular hypertrophy near the ventricular septum is also one of the characteristic findings in hypertrophic cardiomyopathy.

Cardiomyopathy, Dilated↗
PubMed1991

Differentiating cardiomyopathy of coronary artery disease from nonischemic dilated cardiomyopathy utilizing positron emission tomography.

To determine if imaging of blood flow (using N-13 ammonia) and glucose metabolism (using F-18 2-deoxyglucose) with positron emission tomography can distinguish cardiomyopathy of coronary artery disease from nonischemic dilated cardiomyopathy, 21 patients with severe left ventricular dysfunction who were evaluated for cardiac transplantation were studied. The origin of left ventricular dysfunction had been previously determined by coronary angiography to be ischemic (11 patients) or nonischemic (10 patients). Images were visually analyzed by three observers on a graded scale in seven left ventricular segments and revealed fewer defects in dilated cardiomyopathy compared with ischemic cardiomyopathy for N-13 ammonia (2.7 +/- 1.6 versus 5 +/- 0.6; p less than 0.03) and F-18 deoxyglucose (2.8 +/- 2.1 versus 4.6 +/- 1.1; p less than 0.03). An index incorporating extent and severity of defects revealed more homogeneity with fewer and less severe defects in subjects with nonischemic than in those with ischemic cardiomyopathy as assessed by imaging of flow (2.8 +/- 1.8 versus 9.2 +/- 3; p less than 0.001) and metabolism (3.8 +/- 3.3 versus 8.5 +/- 3.6; p less than 0.005). Diagnostic accuracy for distinguishing the two subgroups by visual image analysis was 85%. Using previously published circumferential count profile criteria, patients with dilated cardiomyopathy had fewer ischemic segments (0.4 +/- 0.8 versus 2.5 +/- 2 per patient; p less than 0.01) and infarcted segments (0.1 +/- 0.3 versus 2.4 +/- 1.4 per patient; p less than 0.001) than did patients with cardiomyopathy of coronary artery disease. The sensitivity for differentiating the two clinical subgroups using circumferential profile analysis was 100% and the specificity 80%. An index incorporating both number and severity of defects derived from circumferential profile analysis was significantly lower in subjects with dilated cardiomyopathy than in ischemic cardiomyopathy (0.3 +/- 0.8 versus 2.7 +/- 2.4; p less than 0.005). Thus, noninvasive positron emission tomographic imaging with N-13 ammonia and F-18 deoxyglucose is helpful in distinguishing patients with severe left ventricular dysfunction secondary to coronary artery disease from those with nonischemic cardiomyopathy, and a semiquantitative index such as circumferential profile analysis is superior to that of visual analysis alone.

Adult↗
PubMed1989

Hypertensive hypertrophic cardiomyopathy or hypertrophic cardiomyopathy with hypertension? A study of 78 patients.

Hypertensive hypertrophic cardiomyopathy may be a distinctive cardiac condition resulting from hypertension. Alternatively, this disease may represent the coincidence of a common disease, hypertension, with a relatively rare cardiomyopathy. A consecutive series of patients with hypertrophic cardiomyopathy and hypertension were studied and compared with age- and gender-matched patients with cardiomyopathy alone. Thirty-nine patients were identified as having hypertension; they ranged in age from 31 to 84 years (average 60 +/- 13); 82% were greater than 50 years old; 18 (46%) were women. When these patients were compared with the age-matched group with hypertrophic cardiomyopathy alone, there were no clinical or electrocardiographic differences between the two groups. By echocardiography, the hypertensive and nonhypertensive groups had a similar incidence of systolic anterior motion (77 versus 64%, respectively), mitral annular calcification (31 versus 31%), septal thickness greater than 20 mm (56 versus 46%) and outflow tract gradient greater than 20 mm (59 versus 67%). A posterior wall thickness greater than 13 mm was more frequent in the hypertensive group (54%) compared with the nonhypertensive group (31%) (p = 0.02). The findings show that hypertrophic cardiomyopathy with associated hypertension is a disease of the elderly. But, with the exception of thicker walls, the clinical and echocardiographic features of the patients with hypertension were indistinguishable from those of the age-matched and, hence, elderly group of patients with cardiomyopathy without hypertension. These findings suggest that hypertension may make hypertrophy worse, but that it is not the primary cause of the cardiomyopathy. Thus, the condition might be better termed "hypertrophic cardiomyopathy with hypertension."

Adult↗