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Approximately, 70 % of acute myocardial infarctions are known to develop from mild atherosclerotic lesions. Therefore, it is important to evaluate mild coronary plaques to prevent acute coronary syndrome (ACS). The aim of the present study was to investigate the effects of exercise-based cardiac rehabilitation (CR) on mild coronary atherosclerosis in non-culprit lesions in patients with ACS. Forty-one men with ACS who underwent emergency percutaneous coronary interventions and completed a 6-month follow-up were divided into CR and non-CR groups. Quantitative coronary angiography (QCA) was performed using the automatic edge detection program. The target lesion was a mild stenotic segment (10-50 % stenosis) at the distal site of the culprit lesion, and the segment to be analyzed was determined at a segment length ranging from 10 to 15 mm. The plaque area was significantly decreased in the CR group after 6 months, but was significantly increased in the non-CR group ( P < 0.05). The low-density lipoprotein (LDL) cholesterol, LDL/high-density lipoprotein (HDL) ratio and high-sensitivity C-reactive protein (Hs-CRP) levels were significantly reduced in both groups ( P < 0.01). Peak VO in the CR group was significantly increased ( P < 0.01). Changes in the plaque area correlated with those in Hs-CRP in both groups, while that association with those in HDL-C was observed in only CR group. Stepwise regression analysis revealed the decrease in Hs-CRP as an independent predictor of plaque area regression in the CR group. CR prevented the progression of mild coronary atherosclerosis in patients with ACS. [ABSTRACT FROM AUTHOR]

Dilated cardiomyopathy is characterized by dilatation of the left or right ventricle, or both ventricles. The degree of myocardial dysfunction is not attributable to abnormal loading conditions. The infectious-immune theory has long been hypothesized to explain the pathogenesis of many etiologically unrecognized dilated cardiomyopathies. Inflammations followed by immune reactions, which may be excessive, in the myocardium, evoked by external triggers such as viral infections and/or autoimmune antibodies, continue insidiously, and lead to the process of cardiac remodeling with ventricular dilatation and systolic dysfunction. This ultimately results in dilated cardiomyopathy. Hepatitis C virus-associated heart diseases are good examples of cardiac lesions definitely induced by viral infections in humans that progress to a chronic stage through complicated immune mechanisms. Therapeutic strategies for myocarditis and dilated cardiomyopathy have been obtained through analyses of the acute, subacute, and chronic phases of experimental viral myocarditis in mice. The appropriate modulation of excessive immune reactions during myocarditis, rather than their complete elimination, appears to be a key option in the prevention and treatment of dilated cardiomyopathy. The clinical application of an NF-κB decoy and immune adsorption of IgG3 cardiac autoantibodies have been used as immunomodulating therapies and may provide novel approaches for the treatment of refractory patients with dilated cardiomyopathy. Conventional therapeutic agents for chronic heart failure such as β-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and aldosterone antagonists in particular should be re-evaluated on the basis of their anti-inflammatory properties in the treatment of dilated cardiomyopathy. [ABSTRACT FROM AUTHOR]

Patients are diagnosed as having chronic kidney disease (CKD) if estimated glomerular filtration rate (eGFR) is <60 mL/min/1.73 m2. Low eGFR is likely to increase the incidence of cardiovascular events and lead to dialysis. Therefore, it is important to prevent eGFR from decreasing eGFR. However, it still remains unknown whether antihypertensive therapy can prevent low eGFR from becoming even lower and improve eGFR in hypertensive patients with CKD. The authors analyzed the results of the Japan Multicenter Investigation for Cardiovascular DiseaseB (JMIC-B) and investigated the effects of antihypertensive therapy on eGFR. In hypertensive patients with CKD (eGFR <60), eGFR was significantly increased from 51.87±6.21 (n=98) to 57.55±19.00 ( P<.001) after 3 years of antihypertensive therapy. In patients without CKD (eGFR ≥60), eGFR was significantly decreased from 91.84±23.27 (n=682) to 88.95±23.67 ( P<.001). Regardless of the type of antihypertensive drugs used, eGFR was significantly increased in patients with CKD and was significantly decreased in patients without CKD. This paper shows that antihypertensive therapy can improve eGFR in hypertensive patients with CKD. J Clin Hypertens (Greenwich). 2012;00:00-00. ©2012 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Elderly populations are increasingly represented among patients with acute coronary syndrome (ACS), and advanced age has been identified as an important risk factor for death and adverse outcome in patients with ACS treated invasively. Although considerable data have demonstrated a prognostic benefit of early revascularization in ACS particularly in high-risk patients, elderly patients with ACS are treated invasively less often than younger patients because older age is thought to be an independent predictor of mortality after percutaneous coronary intervention (PCI) in ACS. Over the past 5 years, a total of 54 ACS patients over 85 years old were treated. The 6-month survival rate was around 50% in the non-PCI group ( n = 12) and around 80% in the PCI group ( n = 42) ( P < 0.05). Cardiac death occurred in 6 patients in the PCI group and in 6 patients in the non-PCI group. The rates of both cardiac death and all-cause death were significantly lower in the PCI group. The change in ADL score before and 6 months after the procedure was from 1.57 to 1.59 in the PCI group and from 2.25 to 2.20 in the non-PCI group. PCI for elderly patients with ACS is safe and life saving, and does not reduce the ability to perform activities of daily living. PCI should be recommended even for octo-nonagenerians with ACS. [ABSTRACT FROM AUTHOR]

Recent advances in interventional devices and technology have greatly improved the results of percutaneous transluminal angioplasty (PTA), and it is now being widely used. However, it is important to obtain information regarding its results and its long-term patency. We examined the primary success rates and long-term patency in 29 limbs out of 27 patients with superficial femoral artery (SFA) occlusion who underwent PTA with self-expandable stents. Among the 29 lesions, 19 were long occlusions (>10 cm) and 10 were short (<10 cm). Overall primary success was achieved in 26 of the 29 limbs (90%). There were three unsuccessful cases in which the patients were on dialysis and had hard calcification in the arterial walls. After 3 years, primary patency, primary-assisted patency, and secondary-assisted patency were 81%, 86%, and 96%, respectively. In the case of short occlusions (<10 cm), the 3-year patency was 100%. Both the primary success rate and the long-term patency were considerably better than expected. Our results with self-expanding stents were superior to previously reported results and were not inferior to those of surgical bypass. Therefore, PTA may be considered as a good first option for the treatment of SFA occlusions. [ABSTRACT FROM AUTHOR]

Congestive heart failure developed in a 42-year-old man who had very mild acromegalic features. Echocardiography showed a marked dilatation of the left ventricle and decreased systolic function. Laboratory examinations revealed the elevated levels of growth hormone and insulin-like growth factor-1 and pituitary microadenoma was demonstrated by magnetic resonance imaging. Although the extensive conventional medical treatment was ineffective, short-term addition of somatostatin analog, octreotide, rapidly improved his cardiac function. After discontinuation of octreotide, further improvement was observed with minimal residual diastolic dysfunction. All medical treatment could be stopped after successful trans-sphenoidal surgery. Early diagnosis and effective treatment is important to reverse the acromegalic cardiomyopathy. [ABSTRACT FROM AUTHOR]

A preface for the October 2006 issue of "Drugs" is presented.

A patient with subcutaneous eosinophilic lymphoid granuloma (Kimura's disease) associated with a high serum IgE level and a marked blood eosinophilia, had a glomerulonephritis with electron dense deposits in mesangial, paramesangial, subendothelial, intramembranous and epimembranous areas. By immunofluorescence, all the glomeruli showed predominant depositions of IgE and IgG along the paramesangial areas and capillary walls together with complement components. The germinal centers in the lymph follicles formed in both the subcutaneous granuloma and the kidney interstitium also contained mainly IgE and IgG but no complement components. These features of this disease suggest that the glomerular lesion is one of the systemic manifestations of Kimura's disease. [ABSTRACT FROM AUTHOR]

Objective: (NZW × BXSB)F1 male mice were used as a model to study the effects of chronic administration of nifedipine and diltiazem on small coronary artery disease and mortality. Methods: 16 week old (NZW × BXSB)F1 male mice were given either nifedipine (n=29) at 20 mg·kg−1·d−1 orally or diltiazem (n=28) at 100 mg·kg−1·d−1 orally in two divided doses until they were 24 weeks old (ie, for 60 d). Age matched control mice were given an equivalent volume of vehicle (n=30). Mice that died received immediate necropsy. After 60 d, all surviving mice were killed and hearts and kidneys were examined histologically. Results: The survival rate at 24 weeks was significantly higher in mice given nifedipine than in the controls (71% and 47%, respectively, p<0.05). The number of mice with myocardial necrosis, scar formation, or both, the percentage of areas of the ventricular wall with myocardial necrosis and scar formation, and the number of mice with small intramyocardial arteries showing ≥ 75% stenosis were all significantly lower in the mice given nifedipine than in the controls. In the mice given diltiazem, there were no such differences from the controls. There was no evidence of significant stenosis or thrombosis in the extramyocardial coronary arteries in any of the mice. Systolic blood pressure and the rate-pressure product at 24 weeks of age, as well as the histological score for glomerulonephritis changes, were significantly lower in mice given nifedipine or diltiazem than in the controls. Conclusions: Despite an equivalent improvement of systolic blood pressure, the double product, and renal disease in nifedipine treated and diltiazem treated mice, only nifedipine prevented small coronary artery disease and increased the survival of (NZW × BXSB)F1 male mice, suggesting that nifedipine prevents occlusive thrombi of small coronary arteries better than diltiazem. [ABSTRACT FROM PUBLISHER]

Study objective – Protective effects of nipradilol, a newly synthesised vasodilating β adrenoceptor antagonist, isosorbide dinitrate, and bunazosin on coronary artery constriction induced by intracoronary injection of acetylcholine were determined by coronary arteriography and compared in vivo in pigs.Design – Acetylcholine (12.5,25,50, 100 and 200 μg) was given into the right coronary artery under left ventricular pacing to maintain constant systemic haemodynamics. Percentage narrowing of the major epicardial coronary artery was used as an indicator of constriction of the large coronary arteries, and the time required for the contrast medium to reach the posterior descending coronary artery from the ostium of the right coronary artery (blood flow delay) was used as an indicator of constriction of the small coronary arteries.Subjects – 15 farm pigs weighing 80 to 90 kg were used.Measurements and main results – A marked blood flow delay of over 7.0 s (control: ≤1.8 s) with less than 34% narrowing of the epicardial major coronary artery was observed in 13 of 15 pigs with 12.5-50 μg of acetylcholine, and in the other two pigs with 100 μg of acetylcholine. When marked blood flow delay occurred, the perfused right ventricular myocardium became macroscopically anaemic (ischaemic). Over 75% narrowing of the major epicardial coronary artery was induced in six of the 15 pigs, and over 50% narrowing in 12, with marked blood flow delay with 100 to 200 μg of acetylcholine. However, after intracoronary infusion of 10 μg of nipradilol, acetylcholine induced narrowing in the epicardial major coronary artery was significantly reduced from 44- 79% in control to 19-37% despite 200 μg of acetylcholine, though the time delay in coronary blood flow did not change significantly. By pretreatment with intracoronary isosorbide dinitrate (2.5 mg), the percent narrowing of the large coronary artery and the time delay in coronary blood flow were signifcantly reduced (narrowing from 32-84% to 10.27%; time delay from 7.6-41.6 s to 2.7-22.7 s). Pretreatment with intracoronary bunazosin, an α 1 adrenoceptor antagonist (100 μg), showed no protective effect on narrowing of the epicardial major coronary artery or blood flow delay.Conclusions – Isosorbide dinitrate prevents coronary artery constriction induced by acetylcholine in swine. Nipradilol prevents large, but not small, coronary artery constriction, probably through a direct nitrate like vasodilating action. [ABSTRACT FROM PUBLISHER]

Diffuse coronary artery vasoconstriction was provoked in the rabbit by a stable thromboxane A2 analogue, STA2 (9, 11-epithio-11,12-methano thromboxane A2). Injection of 25 μg·kg−1 STA2 into the left main trunk caused complete occlusion of the left anterior descending artery and narrowing of the left circumflex artery. Two minutes after injection, however, the diameter of the coronary artery returned to the control value (n=10). The right coronary artery was also temporarily occluded by an injection of 25 μg·kg−1 STA2. Left ventricular end diastolic pressure increased significantly, and ST segment elevation of the electrocardiogram occurred during vasoconstriction. The angiographic findings showed that the vasoconstriction in the coronary artery induced by STA2 was similar to the diffuse vasoconstriction seen clinically. Induction of the vasoconstriction by STA2 was prevented by the preadministration of 25 μg·kg−1 of either a calcium antagonist, diltiazem, or a thromboxane A2 receptor antagonist, ONO 3708 (n=10).The relation of the calcium movement to this vasoconstriction was studied in vitro using the isolated left circumflex artery in the rabbit. STA2 (50 μg·litre−1 to 0.5 mg·litre−1) produced a concentration dependent contraction of helical strips of left circumflex artery. Diltiazem (50-100 g·litre−1) suppressed this contraction dose dependently. ONO 3708 (10 μg·litre−1 to 1 mg·litre−1) caused a significant rightward and downward shift of the dose-response curve. A lowering of the concentration of calcium in the incubation medium from 2.54 mmol·litre−1 to 0.01 mmol·litre−1 caused a significant reduction in the STA2 (0.5 mg·litre−1) induced contraction. STA2 (100 μg·litre−1) did not induce a contraction in the absence of external calcium, but the addition of calcium to the incubation medium caused an abrupt contraction. Furthermore, serotonin antagonist, alpha blocker, and angiotensin II analogue had no influence on the STA2 induced contraction. Thus it was concluded that this vasoconstriction was provoked by the increased transmembrane calcium influx induced by STA2. [ABSTRACT FROM PUBLISHER]

To clarify the role of the immune system in the development of myocarditis, BALB/c-nu/nu mice (group l),BALB/c-nu/+ mice (group 2), BALB/c-nu/nu mice injected with 5 × 107 spleen cells from BALB/c-nu/+ mice (group 3), and BALB/c-nu/nu mice injected with 5 × 107spleen cells from BALB/c-nu/+ mice treated with rat anti-Thy-1.2 monoclonal antibody with complement (group 4) were inoculated with encephalomyocarditis virus. There were no significant differences in the incidence of myocarditis among the four groups. Virus titrations of the heart and serum neutralising antibody titres in the four groups did not show any significant differences. Fifty two per cent (26/50) of group 2 and 43% (20/46) of group 3 died on days 9-15, when congestive heart failure developed. Only 9% (5/54) of group 1 and 8% (1/12) of group 4, however, died on days 9-15. Pathological examination confirmed congestive heart failure in groups 2 and 3 but not in groups 1 and 4. Dilatation of the ventricular cavities, pleural effusion, ascites, and congestion of the lungs and liver were present in groups 2 and 3 but not in groups 1 and 4. Cellular infiltration and myocardial necrosis were severe in groups 2 and 3 but minimal in groups 1 and 4. Thus the severity of myocarditis may be regulated by T cells. So-called silent myocarditis seen in clinical settings may be similar to myocarditis in BALB/c-nu/nu mice. [ABSTRACT FROM PUBLISHER]

In a study of the time of appearance of mural thrombus and the relation between thrombosis and congestive heart failure in acute viral myocarditis 180 BALB/c mice were inoculated intraperitoneally with the M variant of encephalomyocarditis virus. Thirty mice were killed on day 5 and 50 mice each on days 7, 10, and 14. Of the 176 mice with myocarditis, 25 (14.2%) developed congestive heart failure after day 9 and 22 (12.5%) showed thrombi after day 6. Most of the thrombi were at the sites of endocardial lesions in the atria. The total incidence of thrombosis in mice with congestive heart failure was significantly higher than that in mice without. None of the 50 uninoculated control mice developed thrombi.The present study suggests that acute viral myocarditis carries an appreciable risk of thromboembolism and that congestive heart failure is a risk factor for thrombosis. [ABSTRACT FROM PUBLISHER]

Positron emission tomography (PET) with C-11 palmitate has been used in estimating the myocardial utilization of free fatty acid. To assess the metabolic reserve in normal subjects, a PET study was performed at control and during dobutamine infusion at 2 hour intervals in 5 normal subjects. Following monoexponential curve fitting of the time activity curve of the myocardium, the clearance half time (min) and residual fraction ( %) were calculated as indices of β-oxydation of free fatty acid. A significant increase in the heart rate and systolic blood pressure were observed during dobutamine infusion (65 ± 5 vs 100±29 bpm, p< 0.05 and 119±12 vs 144±16 mmHg, p< 0.01, respectively). The clearance half time and the residual fraction were significantly decreased (23.4±2.6 vs 15.8±2.3 min and 67.0±2.5vs 58.6± 4.0%, p< 0.05, each). When the left ventricular myocardium was divided into 4 segments, these indices were similar at control and uniformly decreased without regional differences during dobutamine infusion. These data suggest that β-oxydation of free fatty acid may be uniformly increased in the left ventricular myocardium in relation to the increase in cardiac work in normal subjects. PET with C-11 palmitate at control and during dobutamine infusion is considered to be promising in assessing metabolic reserve in the myocardium. [ABSTRACT FROM AUTHOR]

Nitric oxide accounts for the activity of endothelium-derived relaxing factor, which seems to have an important role in vasodilation and inhibition of platelet aggregation. In endothelial cells, one isoform of nitric-oxide synthase is constitutively expressed. Analysis of the cDNA encoding the human endothelial nitric-oxide synthase revealed that the mRNA is 4.1 kb in size and that the translated protein consists of 1203 amino acids. We have cloned a genomic DNA encoding the human endothelial nitric-oxide synthase and analyzed the entire nucleotide sequence of the gene. The gene consists of 26 exons with a total size of 21 kb. The 5′ flanking region of the gene lacks TATA boxes, but it contains putative Sp1-binding sites in (G+C)-rich regions. Of particular interest is the fact that a shear-stress-responsive element is located at position -985, which probably regulates the nitric-oxide- synthase gene in response to fluid mechanical forces at the transcriptional level in the vascular endothelium. Two minisatellite sequences are detectable in introns 2 and 8; a 32-bp consensus sequence repeats 38 times and a 57-bp consensus sequence repeats ten times. We found polymorphisms of the BamHI fragment containing the former minisatellite sequence in genomic DNA from pedigree family members. Furthermore, five tandem repeats of a 27-bp core consensus sequence and 35 repeats of a dinucleotide (CA) are located in introns 4 and 13, respectively. These repeat sequences will probably provide genetic markers for gene mapping and linkage analysis of inherited diseases including cardiovascular diseases. [ABSTRACT FROM AUTHOR]

The effect of beta-blockade in dilated cardiomyopathy was studied by a questionnaire survey. Thirty-three cases were monitored in whom metoprolol (22 patients, 35.9 ± 20.4 mg, mean ± SD), propranolol (four patients, 26.3 ± 7.5 mg), or other beta-blockers (seven patients) were administered. Four patients died, but no direct relationship was found between administration of beta-blocker and death. The NYHA functional class improved significantly. The mean heart rate decreased from 96/min to 77/min ( P < 0.01). The mean cardiothoracic ratio decreased from 55.6% to 52.1% ( P < 0.01). The mean ejection fraction of the left ventricle measured by echocardiogram increased from 30.4% to 36.9% ( P < 0.01). Exercise tolerance in the treadmill test improved significantly. There was no change in blood pressure, nor were there arrhythmias seen on Holter electrocardiograms. In two patients, congestive heart failure deteriorated after administration of beta-blockers. It is concluded that beta-adrenergic blockade has a beneficial effect in most of the patients with dilated cardiomyopathy. [ABSTRACT FROM AUTHOR]

In order to clarify the pathogenesis of acute myocardial infarction (MI) in hearts with normal coronary arteries, infarct size, and the extent of contraction band necrosis (CBN), coagulation necrosis, and hemorrhage were quantitatively examined using an image analyzer in 5 autopsy cases of MI with normal or nearly normal extracardiac coronary arteries. One patient died 40 h after acute MI. A second patient with acute MI due to severe spasm of segment 6, confirmed by cineangiography, died three days later. The third patient had already suffered a subarachnoid hemorrhage, and died 10 h after the onset of acute MI. The fourth patient had aortic stenosis and regurgitation. She developed acute MI due to total occlusion of segment 6, confirmed by cineangiography 4 h after the onset, and died 61 days later. Autopsy revealed old anteroseptal MI with normal coronary arteries and valvular thrombi. The fifth patient had a malignancy, and died one day after the onset of acute MI. Autopsy revealed multiple occlusive thrombi in the small intramural coronary arteries of the left ventricular wall supplied by segment 14, without any stenosis in the feeding vessel. Most infarcts were localized in the territory supplied by 1 or 2 of the 3 epicardial coronary arteries, and coincided with the clinically diagnosed infarct site. The infarct size ranged from 3%-26% of the left ventricular wall, and infarcts were generally localized to the inner third of the wall (67±20%). Histological examination of the four patients with acute MI revealed diffuse CBN (86±14% of the infarcted area) and/or hemorrhage. The findings suggested that MI associated with normal coronary arteries was caused by transient coronary arterial occlusion due to spasm and/or thromboembolism, with the CBN seen in these hearts representing reperfusion injury. [ABSTRACT FROM AUTHOR]

The hemodynamic and clinical effects of OPC-8212, a newly synthesized, orally effective inotropic agent, were assessed for the first time in ten patients with severe congestive heart failure by means of right heart catheterization with a Swan-Ganz catheter. Cardiac output was determined by the thermodilution technique. Patients received a single oral dose of 6 mg/kg. To determine the magnitude and time-course of the effects of OPC-8212, measurements were made during an observation period before and 2, 4, 8, and 12 h after administration. Blood was also taken at these times for measurement of the concentration of plasma OPC-8212. No large meals were allowed during the first 4 h. After the single oral dose of OPC-8212, plasma concentrations increased rapidly, reaching an effective level after 8 h and peaking at 12 h. Hemodynamic performance improved as the mean OPC-8212 plasma level increased, with the maximum effect being observed between 8 and 12 h after acute administration of the drug. At 8 h, the cardiac index was increased from the baseline value of 2.4±0.2 (SEM) to 2.8±0.3 l/min/m ( P<0.01). The stroke work index rose from 26.2±5.1 to 31.7±60 g · m/m. The excessive pulmonary artery diastolic pressure fell from 22±2 to 17±3 mmHg at 8 h ( P<0.001) and to 16±2 mmHg ( P<0.001) at 12 h. The incidence of ventricular premature beats was not increased and no other side effects were observed. These changes were not associated with significant changes in heart rate or systolic blood pressure. Thus, this drug appears to be very promising for the long-term treatment of congestive heart failure. [ABSTRACT FROM AUTHOR]

The effects of nifedipine on regional dysfunction during pacing-induced ischemia were studied in eight patients with coronary artery disease. Single-plane left ventriculograms were obtained using a high-fidelity micromanometer-tipped catheter in the control and post-pacing periods both before and after pretreatment with nifedipine. All patients developed typical anginal pain during pacing tachycardia before but not after pretreatment with nifedipine. After pacing, left ventricular end-diastolic pressure (EDP) increased from 10±5 (SD) mmHg to 23±9 mmHg ( P<0.01) with enlargement of the end-diastolic volume (EDV). The ejection fraction (EF) was reduced from 66±10% to 54±13% ( P<0.05). With nifedipine, a post-pacing increase in EDP was markedly attenuated together with a 17% reduction in left ventricular systolic pressure ( P<0.05). The regional myocardial function was expressed by a radial coordinate system with its origin at the center of gravity of the end-diastolic contour. Two representative radial grids for normal and ischemic segments were selected. In the normal segment, the end-diastolic length (EDL) was augmented by 14% (from 26.1±5.2 mm to 29.7±6.1 mm, P<0.01) associated with a 23% increase in stroke excursion ( P<0.05) with pacing stress. In the ischemic segments, EDL remained unchanged in the post-pacing beat but stroke excursion was significantly reduced (from 11.4±5.2 mm to 4.3±1.8 mm, P<0.01). After pretreatment with nifedipine, the responses of the regional myocardium to the same pacing stress were markedly reduced; the EDL of the control segment was 27.4±4.6 mm with equally augmented stroke excursion. EDL of the ischemic segment remained unchanged but post-pacing deterioration of segment shortening was remarkably improved (8.7±3.3 mm, P<0.05). With pacing stress before nifedipine, the control segment moved up to the higher portion of the single curve. In the ischemic segment, the diastolic pressure became higher at any given length and the pressure length curve clearly shifted upward, indicating regional alteration of the diastolic property. After nifedipine, this upward shift of the regional myocardial pressure-length relationship was markedly attenuated. Thus, we conclude that nifedipine favorably modifies the symptomatic and hemodynamic responses to transient ischemia due to pacing stress largely mediated by selective improvement of the ischemic segment. [ABSTRACT FROM AUTHOR]

To assess the time-course of adaptive responses of the left ventricle to chronic volume overload, dogs were instrumented with a left ventricular (LV) micromanometer and pairs of ultrasonic crystals for the measurement of LV wall thickness (WTh), LV chamber diameter (D), and longitudinal segment length (L). Following a control study, mitral regurgitation (MR) was created by a transventricular section of the chordae tendineae. Heart rate was controlled during each study by atrial pacing. Plasma norepinephrine levels at rest were determined by high-performance liquid chromatography. Eight days (mean) after the onset of MR, end-diastolic (ED) D had increased by 9% from 34.2±2.4 mm (SEM) ( P<0.001), wit significant thinning of the wall thickness (from 8.2 to 7.7 mm, P<0.001). Consequently the calculated cross-sectional area (CSA) of the left ventricular wall remained the same. Peak wall stress (WSt) and EDWSt increased by 20% and 152%, respectively. During the subsequent 4 weeks, EDD progressively increased, averaging 11% above the control at 4 weeks, while EDWTh returned to the control level. Thus, the development of hypertrophy was clearly evidenced by an increase in CSA (by 8% over the control, P<0.001). These changes were accompanied by a consistent reduction in both peak WSt and EDWSt. Mean velocity of circumferential fiber shortening (meanVcf) and percentage shortening were significantly augmented following the onset of MR and remained at the same level thereafter, indicating no further use of the Frank-Starling mechanisms during chronic ventricular dilation. Despite a progressive increase in diameter, longitudinal segment length did not increase throughout the study, suggesting that the ventricle assumes a more globular appearance, as an additional compensatory mechanism to prevent excessive enhancement of diastolic wall stress, Initially elevated plasma norepinephrine concentrations (from 127±28 to 256±69 pg/ml, P<0.05) tended to decrease with the development of hypertrophy (202±55 pg/ml). These data support the view that hypertrophy and change in shape of the left ventricle take place during the course of chronic adaptation to volume overload and normalize the elevated wall stress as a negative feedback. Along with the decrease in wall stress, the initially enhanced sympathetic activity decreases gradually during adaptation to chronic volume overload. [ABSTRACT FROM AUTHOR]

To assess the value of myocardial-perfusion positron computed tomography (PCT) for the evaluation of coronary artery disease (CAD), N-ammonia PCT using a whole-body multislice PCT device was performed at rest and during exercise in 6 normal subjects and 19 patients with angiographically documented CAD. The N-ammonia distribution in the myocardium was assessed both qualitatively and quantitatively. At rest and during exercise, the tracer distribution was homogeneous in the 6 normal cases. In the 19 patients with CAD, regional hypoperfusion was observed in 14 cases (74%) at rest and in 18 cases (95%) during exercise. Additional perfusion abnormalities were detecting during exercise in 12 cases. Segmental analysis of the myocardial perfusion identified 30 out of 34 stenosed vessels (88%) during exercise, with only one false-positive finding of diseased vessels (specificity, 98%). For the quantitative analysis of myocardial perfusion by PCT, the percentage of change in the tracer concentration in the same region between the rest and stress images was calculated. The concentration was slightly increased in normal myocardial segments (14.4%±5.8%; P<0.001), whereas in CAD, it was significantly decreased in segments with stenosed vesels (-18.0%±18.3%; P<0.02). We conclude that N-ammonia PCT at rest and during exercise provides highquality images, and is a sensitive and effective technique for detecting CAD and identifying individual stenosed vessels. Furthermore, this technique makes possible quantitative assessment of the coronary reserve function. [ABSTRACT FROM AUTHOR]

A multigated blood-pool study was performed to assess regional and global emptying and filling in 16 patients with hypertrophic cardiomyopathy (HCM), 43 patients with ischemic heart disease (IHD), and 14 controls. The regional volume curve was fitted using second-order harmonics in the Fourier series, while the global left-ventricular volume curve was fitted using third-order harmonics. As asynchronous indices, the standard deviations (SD) in distribution histograms of time to end-systole (TES), time to peak ejection (TPE), and time to peak filling (TPF) were obtained in the left ventricle. In patients with IHD, the TPF-SD was higher (14.4±11.3°) than the TES-SD (7.8±5.1°) and TPE-SD (8.1±5.9°), suggesting the presence of asynchronous filling. In patients with HCM, the TPF-SD was also higher (11.6±11.1°) than the TES-SD (3.5±2.4°) and TPE-SD (6.2±4.4°). The phase delay was localized in the anteroseptal or apical region in all 5 HCM patients with abnormal wall motion, while it corresponded with the region of abnormal wall motion in the patients with IHD. The TPF-SD was inversely correlated with the left-ventricular ejection fraction ( r=-0.46), peak filling rate ( r=-0.50), and the ratio of peak filling rate to peak ejection rate ( r=-0.52), suggesting that asynchronous filling is related to global diastolic disturbance. We conclude that asynchronous filling is often present in patients with IHD and HCM, and that our technique can be used to obtain a quantitative assessment of regional asynchronous emptying and filling in these diseases. [ABSTRACT FROM AUTHOR]

The value of stress thallium 201 myocardial emission computed tomography (ECT) in the assessment of coronary artery disease (CAD) was analyzed in 75 patients admitted for coronary arteriography. The ECT provided contiguous transaxial, short-axis, and long-axis sections of the myocardium and the myocardial images were divided into nine segments. The sensitivity and specificity in the diagnosis of CAD were 95% and 93%, respectively. Using selected segments, the ECT identified 97 of 111 (83%) major vessels involved: 89% for right coronary artery (RCA), 88% for left anterior descending (LAD), and 70% for left circumflex (LCx). Among the 75 cases, 35 underwent stress conventional planar imaging within 3 months. The planar imaging provided high sensitivity (90%) and specificity (100%) for the detection of CAD patients as well, but it showed lower sensitivity (57%, P<0.001) in identifying individual vessels involved: 55% for RCA ( P<0.01), 70% for LAD, and 36% for LCx ( P<0.05). Stress ECT detected vessel involvement more in two-vessel disease (85%) and three-vessel disease (78%) than the planar imaging (50%: P<0.05 and 44%: P<0.01, respectively). Thus, segmental analysis of stress ECT yielded as high sensitivity and specificity in the diagnosis of CAD as the planar imaging. This can improve sensitivity in identifying individual vessels involved in deep myocardial regions, especially in those with multivessel disease. [ABSTRACT FROM AUTHOR]

To depict the three-dimensional distribution of Tc-pyrophosphate in the heart, emission computed tomography (ECT) was performed, following the conventional planar imaging, in 32 cases with suspected acute myocardial infarction (AMI). There were 23 cases with evidence of AMI, 7 with unstable angina (UA), and 2 with dilated cardiomyopathy (DCM). While the planar images showed discrete cardiac activity in only 11 of the 23 cases (48%) with AMI, the ECT images delineated focal myocardial uptake clearly in 20 of them (87%). On the other hand, the ECT images revealed cardiac blood-pool activity without significant myocardial uptake in all cases with UA and DCM in which the planar images showed diffuse activity. Thus, the ECT imaging of Tc-pyrophosphate seems to be a valuable technique for assessing the presence and localization of myocardial necrosis, especially in cases showing diffuse cardiac activity in the planar imaging. [ABSTRACT FROM AUTHOR]

The pancreatic uptake of Tc stannous pyrophosphate (Tc-PYP) in acute pancreatitis in mice induced by coxsackievirus B3 was studied. Tc-PYP uptake ratio, measured by the ratio of counts/min/g for the pancreas to counts/min/g for the skull, began to increase 2 days after virus inoculation and markedly increased on day 3 when necrosis of pancreatic acinar cells was evident. On day 5, Tc-PYP ratio reached a maximum (2.95±1.85, mean±SD) and histologically fine granules of calcification were seen in teh necrotic acinar cells. Thereafter, cellular infiltrations increased and were most severe on day 7, but Tc-PYP ratio had began to decrease. On day 28, the necrotic areas of the pancreas were replaced with fatty cells and calcification was still present, though Tc-PYP ratio had decreased. The present findings may provide a basis for Tc-PYP imaging in cases of clinical viral pancreatitis. [ABSTRACT FROM AUTHOR]

Fractional myocardial uptake of thallium-201 was estimated by routine scintigraphic evaluation at rest and during exercise in 10 control subjects, 15 patients with coronary artery disease (CAD) and 12 patients with hypertrophic cardiomyopathy (HCM). Fractional myocardial uptake of the total dose administered at rest was 3.59±0.98% in the controls, 4.43±1.17% in patients with CAD and 5.68±1.29% in patients with HCM, and uptake during exercise was 5.07±1.23% in the controls, 4.67±1.04% in the CAD group and 7.50±1.68% in the HCM group. The value in the HCM group was significantly higher than in the controls ( P<0.001 at rest) or in the CAD group ( P<0.02 at rest). A percentage increment of fractional uptake during exercise was significantly smaller in the CAD group than in the controls or the HCM group ( P<0.01). Thus, assessment of the fractional uptake appears to be a valuable adjunct to myocardial imaging when attempting a clinical assessment of CAD or HCM. [ABSTRACT FROM AUTHOR]