Transmural Changes Research Articles

Breath-Hold Dobutamine Magnetic Resonance Myocardial Tagging: Normal Left Ventricular Response

Analysis of the changes in myocardial deformation produced by adrenergic stress has been limited by the imaging techniques used. We used rapid magnetic resonance imaging (MRI) myocardial tagging to map the dose-dependent response to incremental dobutamine in the normal human left ventricle. Thirteen volunteers underwent breath-hold tagged cine MRI during dobutamine infusion. Images were acquired throughout systole to a peak dose of 20 μg/kg/min. End-systolic percent circumferential shortening (%S) was measured at 3 transmural locations and 4 circumferential locations at 3 long-axis positions. Mean circumferential shortening velocity (CSV) was also calculated at each location and dose. Mean %S reached a maximum of 26 ± 3% at 10 μg/kg/min compared with 21 ± 4% at baseline (p <0.003). Peak %S was reached by 10 μg/kg/min before a significant increase in heart rate or blood pressure and was unchanged at higher doses. In contrast, CSV increased linearly with dobutamine dose from 4.4 ± 0.9 mm/s at baseline to 9.8 ± 1.4 mm/s at 20 μg/kg/min (p <0.0001). Breath-hold tagged dobutamine MRI is safe and effective in detecting regional and transmural changes in function during incremental dobutamine. CSV increased continuously across the dobutamine dose range. At low dose (≤10 μg/kg/min) %S increased without any change in blood pressure or heart rate. Maintenance of peak %S beyond 10 μg/kg/min in the presence of decreasing systolic intervals resulted from a continued increase in CSV. Thus, CSV may be the preferred measure of contractile function during dobutamine stimulation in human myocardium.

Local repolarization abnormalities induced by transcatheter radiofrequency ablation in pigs.

Radiofrequency (RF) ablation alters action potential repolarization of myocardial cells and, theoretically, this should induce ST-T segment changes in the ECG. Since these ECG abnormalities have been rarely reported in patients submitted to RF ablation we assess the ability of the procedure to cause ST-T segment changes in local electrograms. Epicardial ECG mapping was performed in 17 anesthetized open chest pigs submitted to endocardial (n = 9) or to epicardial (n = 8) unipolar radiofrequency ablation (500 kHz, 20 W for 5-10 s). To characterize the cellular electrophysiological alterations induced by RF ablation transmembrane action potentials were recorded at various distances from the ablation lesion; these were compared with seven control pigs. Endocardial RF ablation induced a transient (< 5 min) change of 6.1 +/- 2.4 mV in T wave amplitude (baseline: 12.8 +/- 5.6 mV, P < 0.001) in 141 out of 269 epicardial electrodes. T wave changes were associated with shortening in local activation time (20.1 +/- 2.3 ms at baseline vs 18.5 +/- 2.5 ms at 60 s after ablation, P = 0.03). RF current caused persistent St segment elevation at the center of the ablation lesion with no transmural expansion. Intracellular potentials along a 2-6 mm wide myocardial band bordering the RF lesion lower amplitude (101 +/- 7.0 mV vs 71 +/- 23 mV, P < 0.01) and shorter duration (254 +/- 44 ms vs 156 +/- 29 ms, P < 0.01) than control hearts. The center of the ablation lesion was electrically unexcitable. We concluded that RF ablation alters cellular electrophysiology in small areas surrounding the ablation lesion and this causes short-lasting transmural changes in T 3 wave amplitude and nontransmural ST segment elevation.

Transmural changes in mast cell density in rat heart after infarct induction in vivo.

The cardiac distribution of mast cells was investigated after the induction of acute myocardial infarction in the rat. The left anterior descending coronary artery (LAD) was occluded by ligation in the infarct group, whereas in sham rats only a superficial ligature was placed beside the LAD. Rats of both groups were killed at 4, 7, 14, 21, 35, and 85 days following surgery. Hearts were excised and formalin-fixed. Mast cell densities were monitored in subepicardial and subendocardial layers of the left ventricle (LV) in 6 microns thick toluidine blue-stained cross-sections. In control (non-operated) animals, mast cell densities were comparable in the LV subepicardial and subendocardial layers (1.5-2.0 cells per mm2). Following infarction, the mast cell density at the subepicardial site of the infarction gradually increased, reaching a maximum of 25 cells per mm2 on day 21, while a non-significant increase was observed at the subendocardial site. In the non-infarcted regions, the mast cell density increased transiently to reach a maximum of 7 cells per mm2 on day 35 in the subepicardial layer. Again, changes in mast cell density in the subendocardial layer were non-significant. In the sham group, a gradual increase to 9 cells per mm2 on day 21 and a subsequent decrease to 5 cells per mm2 on day 85 were observed in the subepicardial layers. These findings indicate a massive accumulation of mast cells in the subepicardial layers of the infarcted region and a small but significant effect of the surgical procedure on cardiac mast cell deposition, especially in the outer layers of the left ventricle.

Applicability of small endomyocardial biopsies for evaluation of high energy phosphates and glycogen in the heart

To evaluate variability of biochemical determination of energy stores in endomyocardial biopsies, we compared myocardial contents of high energy phosphates and glycogen in endomyocardial and transmural myocardial biopsies from 12 75-kg pigs before, during, and after cardioplegia. Before cardioplegia, comparable amounts of adenine nucleotides and glycogen were found in left and right ventricular endomyocardial and left ventricular transmural biopsies. Phosphocreatine levels were lower in endomyocardial than in transmural biopsies. Significant correlations were observed between endomyocardial and transmural adenine nucleotide and glycogen contents but not phosphocreatine content. During cardioplegia, myocardial ATP and phosphocreatine contents increased and glycogen concentration tended to decrease. During reperfusion, ATP and glycogen levels decreased, whereas phosphocreatine levels increased remarkably. Transmural changes in left ventricular adenine nucleotide and glycogen levels were reflected in endomyocardial biopsies but those in phosphocreatine were not. By increasing the number of endomyocardial biopsies from one to three, within-subject variance was reduced from 33-47% to 14-23% of total variance whereas four or more biopsies only added minor further reduction in variability. In conclusion, endomyocardial biopsies yield representative estimates of the average myocardial content of adenine nucleotides and glycogen but not of phosphocreatine in the normal heart. Endomyocardial biopsies offer a sensitive estimate of the changes in myocardial adenine nucleotides and glycogen induced by cardioplegia and reperfusion. However, metabolite content in endomyocardial biopsies shows a high variability. Three or more endomyocardial biopsies are necessary to reduce variability to acceptable levels.

A regression model of ultrasound reflectivity from normal myocardium

In this paper the potentialities of back-scattered ultrasound to detect changes in transmural myocardial wall structure have been assessed by using a second order regression model of integrated back-scatter. The model was tested through simulation studies and experimental measurements. The experimental results prove the proposed model attractive to detect physiological transmural changes in myofibre orientation from epicardial to endocardial left ventricular wall.

Endothelium dependent vasodilatation following brief ischaemia and reperfusion in anaesthetised swine

The aim as to compare the responses of intracoronary infusions of ATP, an endothelium dependent vasodilator, with adenosine following brief ischaemia (10 min) and reperfusion in a model of myocardial stunning. In group 1 (n = 6), coronary blood flow and endocardial (endo) and epicardial (epi) percent segment length shortening were measured in the distribution of the left anterior descending coronary artery before and during maximal intracoronary infusions of either adenosine or ATP (20 micrograms.kg-1.min-1). Measurements were obtained before and after myocardial stunning both at control heart rate and during atrial pacing (150 beats.min-1). In group 2 (n = 6), myocardial blood flows by microspheres and arterial-venous lactate and oxygen differences were determined following the same ischaemia-reperfusion protocol to characterise transmural changes in blood flow and metabolism in this model of stunning. The experiments were done on 12 anaesthetised swine, weight 25-39 kg. In group 1, baseline endo and epi segment length shortening were 16(SD 3)% and 14(6)% and following reperfusion were reduced to 10(4)% and 8(6)% respectively (p less than 0.05). Prior to stunning, minimal coronary resistances during adenosine and ATP were 0.81(0.40) and 0.76(0.25) mm Hg.min.ml-1 respectively and following reperfusion were 0.86(0.31) (NS) and 0.85(0.23) (NS) mm Hg.min.ml-1 respectively. Infusion of either vasodilator enhanced function by 30% following reperfusion whereas no such effect was observed prior to ischaemia. In group 2, no maldistribution of blood flow was observed following the same ischaemia-reperfusion protocol to account for this vasodilator enhancement in function. Percent lactate extraction values were 29(11)% and 25(14)% at preischaemic control and paced heart rates respectively, and following reperfusion were lowered to 0(12)% without pacing (p less than 0.05) and -1(34)% during pacing (p less than 0.05). Brief ischaemia and reperfusion in swine induces myocardial stunning without altering the vasodilator responses of either ATP, an endothelium dependent vasodilator, or adenosine. Recruitment in postischaemic segment length shortening was observed during infusions of both vasodilators at a time when maldistribution of flow was not observed. Possible mechanisms include either enhanced washout of lactate from the reperfused myocardium or greater utilisation of substrates during higher blood flows.

A New Method for Evaluating Gastric Ulcer Healing by Endoscopic Ultrasonography

We observed the quantitative estimation of the transmural changes associated with gastric ulcer healing by using endoscopic ultrasonography (EUS). It was possible to diagnose the depth of ulcer by EUS. Forty-eight patients were divided into three treatment groups. Group A (n = 16) was treated with 800 mg cimetidine daily, group B (n = 22) with 20 mg omeprazole daily, and group C (n = 10) with 400 mg cimetidine + 300 mg gefarnate daily. EUS was performed before and after 2, 4, and 8 weeks of treatment. The groups were compared from the viewpoints of endoscopic findings and contraction rate of the length and the cross-sectional area of the ulcer in EUS pictures. The best healing of both the endoscopic and EUS findings was seen in group B. By estimating the changes inside the ulcer, EUS may provide useful information for choice of anti-ulcer agents.

Transmural changes in 5′-nucleotidase and the adenine nucleotide metabolite pool in the early acute myocardial infarct : L.C. Armiger, Y.S. Choong. Department of Pathology, University of Auckland School of Medicine, Auckland, New Zealand

Transmural changes in 5′-nucleotidase and the adenine nucleotide metabolite pool in the early acute myocardial infarct : L.C. Armiger, Y.S. Choong. Department of Pathology, University of Auckland School of Medicine, Auckland, New Zealand

A New Ultrasonic Probe for Endosonographic Imaging of the Upper GI Tract

A new ultrasonic probe (7.5 MHz, diameter 3.7 mm) was used in vitro in 3 gastric resection specimens and in vivo in 12 patients in an attempt to visualize normal and pathological wall structure of the esophagus, stomach and duodenum via the working channel of a gastroscope, and of the biliary tract via the percutaneous approach. In 5 of these patients conventional endosonography was performed. The probe visualizes the normal layer structure and pathological lesions of the upper GI-tract wall, since it can be accurately positioned at the structure of interest under visual control; water is instilled into the hollow organs to improve transmission of the ultrasound beam. Intra- and transmural changes such as blood vessels in the wall of the esophagus and stomach in portal hypertension, or gastric and esophageal tumors were demonstrated. The important advantage of the probe is that it can be used in stenosed or narrowed hollow organs, where conventional endosonography fails. However, the depth of penetration of the ultrasonic beam (10-15 mm) and circumferential imaging of the gastric wall are still inferior to those of conventional endoscopic ultrasound. As the focus distance of the ultrasound probe to the biliary ducts is too small, visualization of the biliary system is incomplete. Technical improvements could make this new probe an irreplacable diagnostic tool in the future.

Transmural gradient of glycogen metabolism in the normal rat left ventricle.

The changes of glycogen metabolism with the location of tissue within the ventricle wall have been explored in the rat myocardium. The hearts were cut in 100 microns thick serial sections and all sections were analyzed for their content in glycogen, glucose-6-phosphate, UDPG and glycogen enzymes and for glucose incorporation into glycogen and for the 2-deoxyglucose uptake after the intravenous injection of the 14C-labelled sugars. The rate of glycogen turnover was significantly higher in the subendocardial myocardium (P less than 0.01) and the levels of glucose-6-phosphate and the total (i.e. a + b) activity of glycogen phosphorylase were significantly higher in the subepicardial tissue (P less than 0.01 in both instances). No significant transmural gradient of UDPG was found and transmural changes of total (i.e. I + D) synthase activity were barely significant. These changes in glycogen metabolism may be related to regional differences in the cardiac work load and to a differentiation of the subendocardial and subepicardial heart fibers.

Pericarditis in acute myocardial infarction.

In 1505 patients with acute myocardial infarction (MI) pericarditis was diagnosed most often in those with anterior transmural ECG changes. Those with pericarditis had a significantly greater hospital mortality and peak serum lactic dehydrogenase (LDH) levels and a greater incidence of left ventricular failure (LVF).