BACKGROUND: The purpose of the study is to estimate the total blood flow in coronary artery bypass grafts. METHODS: In a 3-year period 102 patients having a standardized coronary artery bypass grafting (CABG) with the left internal mammary artery (LIMA) anastomosed to the left anterior descending artery and a sequential vein grafted to the remaining diseased coronary arteries were included in the study, 21 females and 81 males. In females a mean of 3.9 anastomosis (range 2-5) were performed and in males a mean of 4.2 (range 2-6) were performed. Flow in the bypass grafts was measured with the transit-time method before termination of cardiopulmonary bypass. RESULTS: Females: LIMA 31 mL/min, vein graft 74 mL/min (26 mL/min per anastomosis), cumulated flow 105 mL/min. Males: LIMA 31 mL/min, vein graft 93 mL/min (29 mL/min per vein anastomosis), cumulated flow 124 mL/min. CONCLUSION: Conventional CABG may restore half of the normal resting coronary artery blood flow (250 mL/min).
1 To identify the roles of endogenous kinins in prevention of myocardial infarction (MI), we performed the permanent ligation of coronary artery in rats. 2 The size of MI 12, 24, and 48 h after coronary ligation in kininogen-deficient Brown Norway Katholiek (BN-Ka) rats was significantly larger (49.7+/-0.2%, 49.6+/-2%, and 51.1+/-1%, respectively) than that of kinin-replete Brown Norway Kitasato (BN-Ki) rats (42+/-2%, 38.5+/-4%, and 41.5+/-1%). 3 Hoe140, a bradykinin (BK) B(2) receptor antagonist injected (1.0 mg kg(-1), i.v.) half an hour before, and every 8 h after, coronary ligation, significantly increased the size of MI in Sprague-Dawley rats. Aprotinin, a kallikrein inhibitor, which was infused intravenously (10,000 Units kg(-1) h(-1)) with an osmotic mini-pump, significantly increased the size of an MI 24 h after ligation. 4 When evaluated using microspheres, the regional myocardial blood flow around the necrotic lesion in BN-Ka rats 6 h after ligation was reduced more than that in BN-Ki rats with MI by 41-46%. The same was true in Hoe140-treated BN-Ki rats. 5 FR190997, a nonpeptide B(2) agonist, which was infused (10 microg kg(-1) h(-1)) into the vena cava of BN-Ka rats for 24 h with an osmotic mini-pump, caused significant reduction in the size of MI (38+/-3%), in comparison with the size in vehicle solution-treated rats (51+/-3%). The size of MI in FR190997-treated BN-Ka rats was the same as in BN-Ki rats. 6 These results suggested that endogenous kinin has the capacity to reduce the size of MI via B(2) receptor signalling because of the increase in regional myocardial blood flow around the ischaemic lesion.
Aortic valve calcification and stenosis become increasingly common with advancing age. This work aimed at assessing whether a time-dependent reduction of aortic valve area is detectable in an unselected elderly population and whether the rate of reduction can be predicted from clinical or biochemical characteristics.
A population-based prospective echocardiographic follow-up study.
A university hospital.
In 1990, randomly selected persons born in 1904, 1909 and 1914 (total n = 501) underwent a Doppler echocardiographic study of aortic valve and biochemical tests of glucose, lipid and calcium metabolism. In 1993, echocardiography was repeated in 333 survivors of the original cohorts. These individuals constitute the present study population.
Three-year changes in the aortic valve area and velocity ratio (peak outflow tract velocity/peak aortic jet velocity) determined by Doppler echocardiography.
Aortic valve area decreased from a mean of 1.95 cm2 (95% confidence interval of mean, 1.88-2.03 cm2) to 1.78 cm2 (1.71-1.85 cm2) within 3 years (P
BACKGROUND: The relation between QRS changes during exercise and ischemic heart disease is controversial. The present investigation addressed whether exercise QRS changes are related 1) to myocardial ischemia or necrosis, 2) to possibly confounding factors such as baseline QRS size and changes in heart rate and ST magnitude during exercise, and 3) to the location of scintigraphic defects. METHODS: Advanced computerized vectorcardiography (MIDA1000, Ortivus Medical AB, Sweden) was recorded in 71 consecutive patients referred for 201TI exercise myocardial scintigraphy. Maximal exercise tests were performed in the sitting position on a bicycle ergometer. Planar scintigraphic images were obtained immediately after exercise and 4 hours later in three projections, and were evaluated blindly. RESULTS: Exercise QRS changes correlated to baseline QRS size (X, Y, and Z leads; P
Clinical characteristics, myocardial perfusion deficits, and clinical outcomes of patients with non-specific chest pain hospitalized for suspected acute coronary syndrome: a 4-year prospective cohort study.
Although the prognostic role of stress SPECT MPI is generally well established, its value in predicting non-fatal cardiac events in patients with acute, non-specific chest pain (NSCP) remains unclear. The aims of this study are 1) to describe the baseline clinical characteristics and prevalence of myocardial perfusion (MP) deficits, by use of an adenosine stress SPECT MPI, in NSCP patients without known CAD discharged after hospitalization for suspected ACS; and 2) to prospectively describe the 4-year clinical outcome in terms of all-cause and cardiac mortality; hospitalization and coronary revascularization procedures; and cardio-vascular events in patients with and without MP deficits.
We evaluated a series of 272 consecutive patients with acute NSCP and aged 18-75years. ICD10-based registries were used to determine the primary outcome (a composite measure of incident CAD death, ACS, or revascularization) and two secondary outcomes (1. all-cause death; 2. a composite measure of cardiovascular death, ACS, revascularization, or stroke). Forty two (15%) participants had a MP deficit. During follow-up (median 1361days), 7 participants had a primary event, 4 died, and 20 had a secondary composite event. Annual event rates were 0.70, 0.39 and 2.07, respectively. MP deficits predicted both subsequent primary and composite secondary events (HR: 7.54; 95% CI=[1.69; 33.69] and 2.93 (95% CI=[1.10; 7.81], respectively). Usual clinical cardiac risk classification could not meaningfully differentiate between patients with and without MP deficits.
SPECT MPI substantially improved prediction of incident CAD beyond usual clinical procedures and risk classification systems among NSCP patients.
The aim of this study was to investigate coronary vascular responses, particularly NO-dependent, in the non-ischemic miocardium during local acute myocardial ischemia/reperfusion. The experiments were performed on the dogs with closed chest. Occlusion of a branch of the coronary artery resulted in a dilatation of the coronary vessels within the intact part of the myocardium. Neither inhibition of prostanoid production and KATP-channels, nor administration of atropine sulfate and dissection of the vagus nerve altered coronary dilatation within the non-ischemic myocardium. Whereas inhibition of NOS by L-NNA (50 mg/kg) completely changed it after coronary occlusion, furthermore coronary resistance temporally increased. Thus, the most reliable mechanism of that response was NO-dependent.
BACKGROUND: Assessments of compromised myocardium and infarct size early after thrombolytic treatment in acute myocardial infarction (AMI) are important for risk stratification and for treatment management. We have therefore evaluated the clinical usefulness of myocardial perfusion scintigraphy (MIBI-SPECT) for the assessment of myocardial viability early after AMI. METHODS: Seventy-one patients [53 men and 18 women, aged 64 +/- 9 years (range 45-75 years)] with AMI treated by thrombolysis took part in this prospective study at University Hospital, Stockholm, Sweden. Sixty of them underwent adenosine-stress and resting MIBI-SPECT 2-4 days after AMI, and 11 were examined only at rest. Six months after the AMI, a repeat MIBI-SPECT at rest was obtained for comparison. RESULTS: All patients had significant perfusion defects compared with an age- and sex-matched healthy reference population. Seventy-six percent of the patients able to undergo a complete adenosine-stress and rest SPECT showed signs of reversible perfusion defects. Defect size (extent) and severity at rest decreased between the tests at 2-5 days and 6 months after AMI (P
Determinants of myocardial hypoperfusion analyzed for the interventricular septum using power Doppler harmonic imaging with contrast echocardiography in humans: a methodologic approach for clinical practice.
BACKGROUND: To evaluate determinants of myocardial hypoperfusion using power Doppler harmonic imaging (PDHI) with myocardial contrast echocardiography (MCE) in clinical practice, a retrospective clinical study was performed comparing echocardiographic and angiographic data. Angiographic data of patients with a normal coronary angiogram (non-CAD) and symptomatic patients with low flow conditions caused by a stenosis of the left anterior descending coronary artery (LAD) or occlusion, or TIMI-II-flow in the LAD were compared with the PDHI data. METHODS AND RESULTS: In 32 patients, MCE was performed with a System Five Performance ultrasound system (GE Vingmed Ultrasound, Horten, Norway). Myocardial perfusion was semiquantitatively analyzed with the EchoPac 6.2b.134 software, bolus injection with Optison (0.35 mL with 5 mL saline flush), and continuous infusion with Levovist (400 mg/mL(-1); 3.5-5 mL/min(-1)) were performed (8 non-CAD patients, 8 CAD patients, respectively). After bolus injection, Doppler intensity (DI) kinetics showed a significant decrease of maximum DI wash-in rate (eg, apical septum [AS]: 4.9 +/- 3.3 vs 2.4 +/- 1.9 dB/s(-1)), of peak maximum DI (eg, AS: 25.3 +/- 6.3 vs 16.4 +/- 5.7 dB), and of DI determined 10 and 20 seconds after peak maximum DI (eg, AS: 22.1 +/- 4.9 vs 10.8 +/- 4.6 dB; AS: 20.4 +/- 5.3 vs 8.0 +/- 3.8 dB, respectively) using a trigger interval once every 3 cardiac cycles when normal perfused areas were compared with hypoperfused areas. During infusion coronary transit time (3.3 +/- 0.9 vs 7.0 +/- 3.6 seconds), maximum DI wash-in rate (eg, AS: 3.2 +/- 1.3 vs 1.3 +/- 0.8 dB/s(-1)) and DI-maximum plateau (eg, AS: 28.6 +/- 4.7 vs 18.3 +/- 6.4 dB) significantly decreased, respectively. CONCLUSION: Regional myocardial hypoperfusion at rest can be detected by using PDHI with MCE in clinical practice, according to a standardized methodologic protocol.
We have determined a release of a stable mitochondrial factor (SMF) into the outflowing blood in vivo. That effect was induced by ischemia/reperfusion or phenylarsin oxide (PAO)--the activators of the mitochondrial permeability transition pore (MPTP) and the oxidative stress. The SMF was measured by a spectrophotometer in the range of wave-lengths 230-260 nm with the absorption maximum of 240-250 nm. The SMF release was accompanied with a decrease in the myocardial contractility, disturbances in cardiodynamics and regional blood circulation. The data obtained have demonstrated that the SMF can be used as a marker of MPTP opening in vivo.
The model of ischemia/reperfusion was reproduced on 9 unconscious dogs. Simultaneously with registration of indexes heart work, hemodynamic and mitochondrial factor (MF) in venous blood from right atrium was defined. Measures were done by spectrophotometria. We have also performed spectrophotometric determination of MF in 11 patients in course of operation with blood cardioplegia. Samples of mixed venous blood from the right atrium were taken on different stages of artificial blood circulation: ischemia and reperfusion. Besides that, patients' level of enzymes was defined: creatine kinase (CK), mv-creatine kinase (mv-CK), lactatedehydrogenase (LDG), aspartataminotransferase (AST), within first day of postoperative period, and also ECG-recording within pre- and after operative period were done. Maximal MF level correlates with frequency and severity of cardiac rhythm disturbance, severity of myocardial hypoxia (r = 0.81). Maximum MF level also demonstrated correlation with KK (r = 0.97), mvKK (r = 0.92), LDG(r = 0.81), AST (r = 0.85). Thus, in experimental and clinic conditions myocardial ischemia was accompanied by mPTP activation, which led to reperfusion myocardial injuries and to release of MF. Method of MF determination gives opportunity to propose its usage as early marker of ischemic injuries and also as marker of mPTP opening in vivo.