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PubMed2006

Effect of etidronic acid on arterial calcification in dialysis patients.

BACKGROUND: Bisphosphonate drugs, including etidronic acid, are effective agents for the treatment of osteoporosis and may reduce arterial calcification. The aim of this randomised control trial was to characterise the effect of etidronic acid on arterial calcification in patients undergoing chronic haemodialysis. METHODS: Patients undergoing chronic haemodialysis were assigned to one of two groups by a simple randomisation method: an etidronic acid group (n = 8; 400 mg/day for 24 weeks) and a control group (n = 6; no etidronic acid therapy). Serum calcium, phosphate, calcium-phosphate product, alkaline phosphatase, lactate dehydrogenase, activated colecalciferol and parathyroid hormone levels were measured at baseline and then at 4-weekly intervals thereafter. RESULTS: Calcification scores of the coronary arteries and the thoracic and abdominal aorta were determined by volume-correcting data collected by a multi- detector-row computerised tomographic scanner at baseline, at 6 months and at 1 year. Two patients in the etidronic acid group were excluded from the final analysis because of medical complications. The remainder of the patients (n = 6) showed no significant temporal changes in serum levels of assessed parameters. While no significant temporal changes in coronary calcification score were observed in either group, the mean aortic calcification score significantly decreased over time from 1000 +/- 460mm(3 )at baseline to 970 +/- 580mm(3) at the completion of treatment and 350 +/- 180mm(3) at 1 year (p = 0.009), corresponding to a mean percentage decrease of -64.1% (range -86.5% to -50.1%). By contrast, in the control group, the mean aortic calcification score significantly increased with time from 1460 +/- 1280mm(3) to 1510 +/- 1150mm(3) at the completion of treatment and 2070 +/- 1200mm(3) at 1 year (p = 0.006), corresponding to a mean percentage change in the calcification score of +130.0% (range 2.1-414%). CONCLUSION: Etidronic acid markedly reduced aortic calcification in patients with end-stage renal disease undergoing chronic haemodialysis. The effect of this agent on aortic calcification may attenuate the increase in aortic stiffness and result in improved long-term outcomes in patients undergoing chronic haemodialysis.

Aged↗
PubMed1982

Incidence of aortic cusp and mitral annulus calcification as determined by echocardiography: significance and interrelationship.

M-mode and two-dimensional echocardiograms of 3,254 patients without evidence of rheumatic heart disease were evaluated retrospectively for evidence of aortic cusp calcification and mitral annulus calcification. Echographic evidence of mitral annulus calcification was found in 6.3% of the patients studied. In 375 patients with echographic evidence of aortic valve calcification, the incidence of mitral annulus calcification was 30.6% and it was more than twice as common in females (44.9%) as in males (19.2%). Mitral annulus calcification in patients with aortic cusp calcification was age- and gender-dependent. It occurred in 25% of women younger than 50, 50% of women over 60, and 60%Q of women over 80 years of age. The incidence in males was 28.5% and 27% in the 70s and 80s, respectively. There was no correlation between the severity of aortic valve calcification of stenosis and the incidence of mitral annulus calcification.

Adolescent↗
PubMed1988

CT of aortic aneurysms: the distinction between mural and thrombus calcification.

Aortic calcification, either mural or thrombus, is a common finding in patients with abdominal aortic aneurysms. Differentiating between the two sites of calcification is necessary in order to avoid confusing simple thrombus calcification with displaced calcified intima in aortic dissection. The CT scans of 145 cases of abdominal aortic aneurysm and seven cases of abdominal aortic aneurysm with dissection were analyzed with respect to the location of the calcification: mural only or mural and thrombus. Mural calcification was seen in all 152 patients with aneurysms whereas thrombus calcification was identified in only 33 (24%) of the 136 patients with thrombus. Displaced intimal calcification caused by aortic dissection can either appear similar to or, at times, be indistinguishable from thrombus calcification. Thrombus calcification was present in four (57%) of the seven patients with abdominal aortic aneurysms and dissection. To avoid the possibility of a false-positive diagnosis of aortic dissection in patients with abdominal aortic aneurysm, other signs of aortic dissection should be sought such as separation of the true and false lumina by an intimal flap.

Adult↗
PubMed1994

CT-detected renal arterial calcification: correlation with renal artery stenosis on angiography.

OBJECTIVE: The purpose of this study was to determine whether a relationship exists between CT-detected calcifications in the main renal artery and renal artery stenosis. We also evaluated whether renal artery calcifications are more indicative of stenosis in particular patient subgroups based on age, sex, or hypertensive status. MATERIALS AND METHODS: We retrospectively reviewed the examinations of 70 patients (122 kidneys) undergoing both abdominal CT and angiography for various clinical conditions, most commonly evaluation of a tumor or aneurysm. CT studies were evaluated for degree of calcification at the orifice and in the proximal and distal segments of the main renal artery. The angiograms were evaluated for degree of narrowing. Renal artery stenosis was defined as a reduction in cross-sectional area of 75% or more. A separate analysis was performed on male and female patients above and below 65 years of age, with and without hypertension. RESULTS: Renal arteries with clumps of calcium (> 3 mm in diameter) had a higher percentage of stenosis (7/16, 44%) than did renal arteries with less calcium (16/53, 30%), and renal arteries with no calcium had the fewest stenoses (9/53, 17%; p = .02). Calcifications in the renal artery were not good predictors of stenosis as they were frequently seen in arteries with nonsignificant narrowing and were occasionally seen in arteries with no narrowing. The patient's sex was not a significant factor in this analysis (p = .34). Renal artery calcifications in hypertensive patients showed a stronger association with renal artery stenosis, but the overall ability to predict stenosis remained poor. However, calcification may be significant in persons less than 65 years old, in whom this finding was associated with stenosis all three cases (100%). Similar calcifications in patients 65 years old or more were associated with stenosis in only 4 (31%) of 13 cases (p < .01). CONCLUSION: CT-detected calcifications in renal arteries are associated with stenosis, but their predictive value in the general population or in hypertensive patients is poor. These calcifications in a patient less than 65 years of age are a better indicator of stenosis of the renal artery.

Calcinosis↗
PubMed1994

Medial artery calcification predicts cardiovascular mortality in patients with NIDDM.

OBJECTIVE: To study the predictive value of medial artery calcification (Mönckeberg's sclerosis) in relation to 10-year cardiovascular mortality in patients with non-insulin-dependent diabetes mellitus (NIDDM). RESEARCH DESIGN AND METHODS: We studied the predictive value of thigh medial and intimal artery calcifications to 10-year cardiovascular mortality in a well-characterized group of 133 middle-aged, newly diagnosed patients with NIDDM (70 men and 63 women). RESULTS: At baseline, medial artery calcifications were found in 17% of the patients and intimal-type calcifications were found in 23%. During the follow-up, 21% of the diabetic patients died from cardiovascular causes. The age-adjusted odds ratio for cardiovascular mortality was 4.2 (95% confidence intervals: 1.5-11.3) for medial-type and 1.6 (0.6-4.3) for intimal-type calcifications. In multiple logistic regression analysis, including age, sex, systolic blood pressure, low-density- and high-density-lipoprotein cholesterol, very-low-density lipoprotein triglycerides, smoking, body mass index, fasting serum insulin, blood glucose, urinary albumin, and ischemic ECG changes, as well as the intimal artery calcification, the medial artery calcification was the dominant factor predicting cardiovascular mortality. CONCLUSIONS: In this study medial artery calcification was a strong independent predictor of cardiovascular mortality in patients with newly diagnosed NIDDM. Whether these subjects had a longer duration of hyperglycemia before the diagnosis than those without medial artery calcifications remains unknown.

Calcinosis↗
PubMed1984

Arterial calcifications in uraemic rats treated with 1-alpha-hydroxycholecalciferol and parathyroidectomy.

The effect of 1-alpha-hydroxycholecalciferol (1-alpha-OH-D3) on the incidence of arterial calcifications, and the influence of parathyroidectomy on the effect of this vitamin D treatment, were studied in uraemic rats. Uraemia was induced by 3/4 kidney resection, and parathyroidectomy was achieved by electrocoagulation. 1-alpha-OH-D3 in a dose of 3, 10 or 125 ng/100 g body weight (b.w.) was given in the drinking water. The animals were killed after 12 or 16 weeks. Aorta and small arteries in the heart and in anterior tibial muscle were studied by light microscopy. Arterial lesions were frequently found in uraemic rats and were characterized by medial necrosis and calcifications. Following a 1-alpha-OH-D3 dose of 125 ng/100 g b.w. in uraemic rats both serum calcium and serum phosphate were increased and there was a high incidence of arterial calcifications both in the aorta and the small arteries. In uraemic rats receiving 10 ng/100 g b.w. of 1-alpha-OH-D3 serum calcium was only slightly elevated although the incidence of arterial calcifications (mainly in the aorta) was such higher than in uraemic rats without vitamin-D treatment. A dose of 3 ng/100 g b.w. of 1-alpha-OH-D3 given to uraemic rats did not result in any serum calcium increase, nor did it alter the incidence of arterial calcifications. Parathyroidectomy prevented arterial calcifications. Parathyroidectomy prevented arterial calcification in uraemic rats, but this effect was abolished by 1-alpha-OH-D3 in a dose of 10 ng/100 g b.w. which only raised the serum calcium to a subnormal value. In uraemia, treatment with 1-alpha-OH-D3 may increase the serum calcium X phosphate product, but this cannot fully explain the increased incidence of arterial calcifications. It is therefore suggested that vitamin D causes changes in the arterial wall which increase its susceptibility to the development of calcifications.

Animals↗
PubMed2003

Characterization of an in vitro model of calcification in retinal pigmented epithelial cells.

Little is known about the relationship at the molecular and cellular levels between vascular calcification and elastic fibers essential for elasticity. To gain a better understanding of the physiological function of elastin in vascular calcification, we developed a calcification model on cultured bovine retinal-pigmented-epithelial cells (RPEs) that do not express endogenous tropoelastin. The addition of inorganic phosphate (NaH2PO4; Pi) induced calcium deposition in RPEs. The Pi-induced calcification, as assessed by the o-cresolphthalein complexone method, Goldenbergs method, and von Kossa staining, was completely inhibited by treatment with clodronate (DMDP) and phosphonoformic acid (PFA) and was weakly suppressed by treatment with levamisole. Moreover, the osteopontin mRNA expression was upregulated in the Pi-induced calcification of RPEs. These reactions in RPEs were characteristically consistent with those already established in cultured bovine aortic smooth muscle cells (BASMCs). Furthermore, bacterially expressed tropoelastin inhibited calcium deposition in RPEs as well as in BASMCs. Finally, Pi-induced calcification was partially suppressed after the addition of tropoelastin due to elastic fiber formation. In conclusion, we suggest that this calcification model in RPEs is useful for analyzing the relation between elastic fibers and vascular calcification, and that tropoelastin and elastic fibers may contribute to the inhibition of vascular calcification.

Animals↗
PubMed2000

Regulatory mechanisms in vascular calcification.

Vascular calcification is increasingly recognized as a significant contributor to cardiovascular morbidity and mortality as well as a biologically regulated process potentially subject to prevention and reversal. Both coronary and aortic calcification are common and influence plaque rupture, angioplasty and surgical complications, and compensatory enlargement. Aortic calcification increases aortic rigidity and contributes to cadiac ischemia, left ventricular hypertrophy, heart failure, and stroke. Calcification is also common in aortic valve leaflets further compounding adverse hemodynamic effects. Vascular calcification has often been attributed to "passive" crystallization. However, functional similarities between atherosclerotic lesions and bone contradict this view and indicate that it is no more "passive" than in embryonic bone formation or bone repair. Similarities include presence of all the major components of bone osteoid, bone regulatory factors, and subpopulations of artery wall cells that retain osteoblastic lineage potential. Several animal models for vascular calcification are available. Spontaneous vascular calcification occurs in null mice for matrix GLA protein (MGP), a small matrix protein of unknown function, and osteoprotegerin (OPG), known to modulate osteoclast differentiation. Vascular calcification may also be induced by feeding vitamin D and calcium or warfarin to normal animals, or by fat-feeding mice null for apoE or the LDL-receptor. Overall, regulation of vascular calcification is a growing field with surprising mechanisms and connections to other fields of biology.

Animals↗
PubMed2001

Fixation-related autolysis and bioprosthetic aortic wall calcification.

BACKGROUND AND AIM OF THE STUDY: It has been established previously that immediate fixation and increased glutaraldehyde (GA) concentrations are required to prevent severe autolytic tissue damage during bioprosthetic aortic root production. The study aim was to verify that structure-preserving fixation also reduces aortic wall calcification. METHODS: Porcine aortic roots were fixed either instantly or after being kept on ice for 48 h (phosphate-buffered saline, PBS). Two concentrations of GA (0.2% and 3.0%) were chosen (4 degrees C, seven days, PBS). Discs of aortic wall tissue (1.2 cm diameter) were implanted subcutaneously in rats for 60 days (n = 10 per group), while aortic roots were implanted in the distal aortic arch of sheep for six weeks (n = 3 per group) and six months (n = 4 per group). Calcification was assessed by atomic absorption spectrophotometry and light microscopy. Fixation-related tissue damage was determined by transmission electron microscopy, and correlated with calcification. RESULTS: No significant difference in calcification was found between immediate and delayed fixation if tissue was fixed with 0.2% GA. In the 3.0% GA group, both animal models showed a significantly lower level of calcification if tissue was immediately fixed. In the subcutaneous rat model, immediate fixation reduced calcification by 26% (p <0.0001). In the circulatory sheep model immediate fixation did not affect calcification in the short-term six-week implants, but markedly lowered it by 37% (p = 0.035) after six months. Ultrastructurally, there was a significant correlation between membrane damage, vacuolization and vesicle shedding on the one hand, and calcification on the other. CONCLUSION: Coincidental fixation-related ultrastructural damage and increased calcification was demonstrated in bioprosthetic aortic wall tissue.

Animals↗
PubMed2004

Ethanol inhibition of porcine bioprosthetic heart valve cusp calcification is enhanced by reduction with sodium borohydride.

BACKGROUND AND AIM OF THE STUDY: Previous studies have shown that ethanol pretreatment of glutaraldehyde (GA)-fixed porcine aortic valve cusps (GPAV) significantly reduces bioprosthetic leaflet calcification. The anti-calcification mechanism is due to extraction of cholesterol and phospholipids, and a permanent alteration in collagen structure. It was noted in experimental implants that ethanol-pretreated GPAV occasionally show low levels of calcification. The study aim was to investigate whether this was due to unreacted aldehyde residues and other reducible compounds resulting from GA cross-linking. METHODS: GPAV were cross-linked in GA (0.6%) and stored at pH 7.4 in 0.2% GA. Cusps were pretreated with ethanol (80%, pH 7.4) for 24 h. Experimental groups included ethanol-pretreated cusps and GA-fixed controls that were pretreated with either sodium borohydride or sodium cyanoborohydride. Differential scanning calorimetry was used to measure shrink temperature as a measure of cross-linking. Subdermal implants of valve cusp tissue were carried out in 21-day-old Sprague-Dawley male rats. Implants were retrieved at 21 days and samples assessed for the extent of calcification using chemical analyses for Ca, and microscopy studies. RESULTS: Ethanol pretreatment significantly inhibited calcification compared with controls (13.3 +/- 5.6 versus 119.2 +/- 6.6 micrograms Ca/mg tissue; p < 0.001). However, sodium borohydride reduction under optimized conditions combined with ethanol pretreatment optimally reduced calcification (1.16 +/- 0.1 microgram Ca/mg; p < 0.05), whereas levels after sodium cyanoborohydride treatment (23.6 +/- 10.4 micrograms Ca/mg) were not significantly different to those after ethanol alone. Neither reducing agent was effective in inhibiting calcification without ethanol pretreatment. Furthermore, the reducing agents had no significant effect on shrink temperature. CONCLUSION: Inhibition of GPAV calcification with ethanol pretreatment can be enhanced through the optimized use of reducing agents. This indicates that reducible aldehyde-related moieties are likely responsible for breakthrough calcification, even after ethanol pretreatment.

Animals↗
PubMedDate not supplied

Middle cerebral artery infarction: relationship of cavernous carotid artery calcification.

BACKGROUND AND PURPOSE: This study was designed to determine whether calcification of the cavernous carotid artery (CCA) is associated with cerebrovascular infarcts in the same way that coronary artery calcification scores indicate myocardial infarctions. We sought to correlate the grade of CCA calcification with infarctions in the middle cerebral artery (MCA) distribution. METHODS: Nonenhanced brain CT scans of 40 patients with MCA-distribution strokes, 34 with non-MCA-distribution strokes, and 94 age-matched control subjects were reviewed. Circumferential calcification and thickness of calcification were graded for the CCAs on head CT scans. Scores were determined for the left and right CCAs. Mann-Whitney tests and Spearman correlation coefficients were used to detect differences between patients and control subjects and between patients with MCA and those with non-MCA strokes. RESULTS: CCA calcification scores did not significantly differ in the groups compared. The manner in which calcification was scored (by using circumference, thickness, or both) did not affect the results. No difference was noted between scores ipsilateral and those contralateral to the stroke. CONCLUSION: Circumferential degree or thickness of cavernous artery calcification was not correlated with MCA or non-MCA infarctions. CCA calcification scores did not differ between patients with stroke and those without stroke.

Adult↗
PubMed1992

Mammographic analysis of calcifications.

Because mammographically detected calcifications are frequently the only sign of breast cancer, the breast radiography equipment, screen-film imaging package, and film processing should be optimized to detect such calcifications. For this purpose, dedicated units with molybdenum targets, microfocal spot magnification capability, reciprocating grids, and high output x-ray tubes are required. With the greater use of state-of-the-art mammography, intraductal carcinoma, or DCIS, manifested only by calcifications is being detected more frequently than ever. DCIS can be of the comedo, cribriform, or micropapillary types. Comedocarcinoma, characterized by linear and branching (casting) calcifications, is the most aggressive type, and it has the highest rate of recurrence after breast-conserving surgery. Cribriform and micropapillary calcifications are characteristically punctate and vary in size and shape. In addition to histologic type, the recurrence of DCIS is related to its extent at detection and whether adequate tissue was removed at the time of breast-conserving surgery. Biopsies for suspicious calcifications should be followed immediately by specimen radiography to verify their removal. If breast-conserving surgery is elected for DCIS, the resected segment of tissue should be examined with pathologic techniques designed to determine whether the margins are clear of tumor. For DCIS and invasive cancers with extensive intraductal component, microfocus magnification mammography over the surgical site is recommended prior to radiotherapy to identify any residual tumor calcifications. Although state-of-the-art mammography is very sensitive in the detection of calcifications, it is low in specificity, thus resulting in a large number of false-positive mammograms and a relatively low true-positive biopsy rate. While some benign calcifications cannot be distinguished from those of malignancy, the number of biopsies for benign conditions can be decreased by careful analysis of the mammograms in a search for features indicating benignity.

Breast Diseases↗
PubMed1990

Pancreatic calcifications in patients with chronic pancreatitis. A sign of long-lasting or severe disease?

Pancreatic calcifications are particularly frequent in patients with severe pancreatic insufficiency and long-lasting chronic pancreatitis. To clarify whether calcifications point to a more severe form of the disease, irrespective of its duration, we have retrospectively analyzed patients with chronic pancreatitis submitted to the secretin-cerulein test in our center over a six-year period. Out of 120 patients, calcifications were found in 55. Higher alcohol intake and longer duration of the disease were found in patients with calcifications, compared with patients without calcifications (p less than 0.001). In both groups, lipase and chymotrypsin were more severely impaired than bicarbonate; a greater reduction of pancreatic exocrine function was found in patients with calcifications, compared to those without (p less than 0.001, Mann-Whitney U-test). When the patients were classified according to the duration of the disease or the severity of exocrine function impairment, higher percentages of patients with calcifications were found in the classes with more advanced disease. A log-linear analysis showed that the prevalence of calcifications was associated with pancreatic function impairment, even within the same class of duration of the disease. It is likely that calcifications mark more severe forms of chronic pancreatitis, even in the early phases of the disease.

Adolescent↗
PubMed1990

Cardiac calcific deposits in patients with primary hyperparathyroidism: preliminary results of a prospective echocardiographic study.

To explain the incidence and significance of mitral and aortic valve calcification and calcific deposits in the myocardium, a prospective echocardiographic study was performed with 21 consecutive patients who had primary hyperparathyroidism (PHP) and with 21 age- and sex-matched control subjects with normocalcemia. Calcific deposits in the myocardium were seen in 13 patients (62%) with PHP, mainly in the interventicular septum, and in one control subject. Aortic valve calcification was observed in 12 patients (57%) with PHP and in one control subject. Calcification of the mitral valve was found in seven patients with PHP (33%) and three controls (14%). Calcification led to mild or moderate stenosis of the aortic valve in three patients with PHP and of the mitral valve in two patients with PHP. No stenosis was found in the subjects in the control group. Both calcification of the aortic and mitral valves and calcific deposits in the myocardium are common in patients with PHP and can be detected noninvasively by echocardiography. Because of the potential relationship of elevated calcium, calcification, and valvular heart disease, clinical evaluation of PHP should include echocardiographic studies before surgery is performed and during follow-up examination.

Adult↗
PubMed1989

CT of aortic and mitral valve calcification.

In a retrospective study of 100 patients 40 years of age or older, routine CT of the thorax demonstrated calcification of the aortic valve in five and mitral valve in five. The prevalence of valvular calcification increased with increasing age; calcification was present in 36% of patients over 70 years of age and 75% over 80. None had a history of rheumatic fever; in nine of 10 cases valvular calcification appeared to be degenerative in etiology. In one younger patient, aortic valvular calcification occurred in a congenitally bicuspid valve. Aortic valvular calcification on CT is specific for aortic stenosis; CT also demonstrates the calcification earlier than either plain radiographs or echocardiography. In the elderly, mitral valve calcification on CT seems to occur as a manifestation of degenerative changes in the mitral valve and anulus and may be associated with mitral insufficiency, mitral valve prolapse, or conduction abnormalities. Two-dimensional echocardiography and doppler interrogation of the valves should be done in any patient in whom CT demonstrates aortic or mitral valvular calcification.

Adult↗
PubMedDate not supplied

The detection of intracranial calcifications by MR.

Twenty patients in whom CT had unequivocally demonstrated the presence of calcification in a diversity of lesions and who had undergone MR, performed at 0.6 T and with standard T1- and T2-weighted pulse sequences, were retrospectively studied to determine the MR signal-intensity characteristics of the calcifications and to assess the ability of MR to detect the presence of this abnormality. CT proved superior to MR in detecting and characterizing calcification. In seven of 20 cases, the apparent extent of calcification was equal by both imaging techniques, and in 13 of the 20 cases, CT showed more extensive abnormality. In five of the 20 cases, the calcifications were seen by MR as regions of profoundly reduced signal intensity, approximately equal to cortical bone, in all pulse sequences. In 12 of the 20 cases, the signal intensity was profoundly reduced in one or more, but not all, pulse sequences. T2-weighted pulse sequences were most sensitive in detecting calcification of signal void. Reviewed without knowledge of the CT findings, the MR images were interpreted as definitely indicative of the presence of calcification in three of the 20 cases. In seven of the 20 cases, the MR images raised the possibility of calcification but were less definitive than the CT findings. In 10 of the 20 cases, MR was judged indeterminate for the presence of calcification.

Adolescent↗
PubMed1988

[A case of pseudohypoparathyroidism with intracerebral calcification].

Intracerebral calcifications, especially in the basal ganglia, are observed in many kinds of diseases. A 41-year-old man is reported, who suffered from an acute epidural hematoma and underwent surgery to remove the hematoma. We detected very extensive intracerebral calcification on CT. Laboratory findings revealed hypocalcemia and hyperphosphatemia. General physical examination revealed characteristics typical of pseudohypoparathyroidism. The patient was diagnosed as having pseudohypoparathyroidism type I by the Ellsworth-Howard test. Since the advent of CT, the incidence of basal ganglia calcification has increased. CT is 5 to 15 times more sensitive than skull radiography in the detection of intracerebral calcification. Although many pathological states can cause basal ganglia calcification, most of the calcifications which are recognized on CT scans are physiological. But in cases in which basal ganglia calcifications are recognized also on plain radiographs, various kinds of symptoms including ones of basal ganglia origin are often recognized, and calcifications often extend to regions other than basal ganglia, eg. cerebellum, thalamus, etc. Pseudohypoparathyroidism is a rare disease which presents hypocalcemia, some characteristic physical appearances, and dementia. It is important to decide whether further examinations are necessary or not, when basal ganglia calcification is recognized incidentally on CT scan.

Acute Disease↗
PubMed1988

[Coronary calcification in cinefluoroscopy: diagnosis of ischemic heart disease masquerading as dilated cardiomyopathy].

The feasibility of cinefluoroscopic grading of coronary calcification was tested for differential diagnosis of ischemic cardiomyopathy (IMD) and non-ischemic myocardial disease (N-IMD) simulating dilated cardiomyopathy (DCM). Twenty-seven patients with generalized hypokinesis of the left ventricle but without localized infarction or aneurysm on two-dimensional echocardiography were categorized as Group A of 17 cases examined by both cinefluoroscopy and coronary cineangiography (CAG); Group B, 10 examined only by noninvasive method because of severe congestive heart failure, old age or poor renal function. Cinefluoroscopy was recorded on 35 mm cinefilm for review using a 7 inch image intensifier, 2 to 3 mA and 90 to 100 kV, in the anteroposterior, right and left anterior oblique, and left lateral projections. We judged the degree of coronary calcification as Grade 1, calcification difficult to recognize; Grade 2, easily recognized; Grade 3, recognized in more than half of one coronary artery; and Grade 4, recognized in nearly the entire length of one coronary artery. To obtain the calcification score, the degree was multiplied by the number of calcified main coronary branches. IMD was defined as more than 75% decrease in the diameter of either the left main coronary artery or any other two major coronary vessels. I. The results obtained for group A were: 1. All six cases of IMD had coronary calcification. 2. The score of IMD was 21.2 +/- 8.1; that of N-IMD, 0.18 +/- 0.39. 3. The minimum IMD score was 10 without evidence of any calcification in the non-dominant right coronary artery. 4. Among three cases of DCM, two scored 1 and one scored 0. 5. The sensitivity and specificity of calcification for IMD were 100% and 81.8%, respectively. II. The following results were obtained in Group B, if IMD was defined as score more than 10. 1. The mean score of three IMD cases was 28 +/- 1.4, and the diagnosis was confirmed by subsequent CAG in two of them. 2. In none of the five N-IMD cases, calcification was recognized. The diagnosis of one case was confirmed by subsequent CAG. 3. The diagnosis was not confirmed in two cases who had score 3. These results indicate that calculated scores based on the severity of coronary artery calcification documented cinefluoroscopically can differentiate IMD from N-IMD both inexpensively and noninvasively.

Adult↗