End-systolic and end-diastolic left atrial volume assessment by two-dimensional echocardiography: a comparison study with magnetic resonance imaging.

BACKGROUND: The left atrial volume (LAV) is an important indicator of the severity of certain diseases, and measuring LAV through the cardiac cycle may enable the evaluation of various left atrium (LA) functional parameters. The results of two-dimensional (2D) echocardiographic LAV measurement methods vary, and no technique is accepted as being optimal. OBJECTIVE: This study compared the accuracy of end-systolic and end-diastolic LAV measurements by 2D echocardiography with those obtained by magnetic resonance imaging (MRI). METHODS: Fifty consecutive patients who underwent both echocardiography and MRI due to clinical reasons with nonselective cardiac disease were studied. LAVs by 2D echocardiography were obtained with the prolate ellipsoid (PE), biplane area-length (AL), and modified Simpson's (MS) methods. RESULTS: End-systolic and end-diastolic LAVs calculated by each method correlated significantly with MRI results (P < 0.0001). The prolate ellipsoid method provided LAVs that most correlated with MRI results, and the biplane area-length and modified Simpson's methods provided LAVs with small mean differences (<5 ml) compared to MRI results. CONCLUSION: All three methods of 2D echocardiographic LAV measurement provide valuable LAV data, suggesting the possibility of evaluating various LA functional parameters.

Comparison of delayed myocardial enhancement in the early and late phase after contrast injection: is it possible to reduce the examination time for myocardial viability study?

OBJECTIVES: We studied whether we can obtain a myocardial viability study immediately after contrast injection to reduce the whole cardiac MR examination time. MATERIALS AND METHODS: We examined 36 patients with cardiovascular abnormality on comprehensive cardiac MRI. T1-weighted images with inversion recovery (IR) were obtained 5 min after stress perfusion with 0.05 mmol/kg of gadodiamide and 15 min after the resting perfusion with the same dose. (The latter images were obtained 25 min after the initial administration.) We evaluated the existence, the number of sectors, and the degree of enhancement at each time. The contrast ratio was also calculated. The number of the enhanced sectors and the contrast ratio were statistically compared using Student's t test. RESULTS: All 17 cases of delayed myocardial enhancement at 25 min after contrast injection showed some enhancement at 5 min after contrast injection. However, the number of enhanced sectors was larger at 25 min after the initial injection in 11 cases, and it was statistically significant (P=.017). The degree of enhancement was stronger at 25 min in 14 cases. However, the contrast ratio at 5 and 25 min after contrast injection was not significantly different (P=.245). CONCLUSION: Myocardial viability study immediately after contrast injection is too early to evaluate the extent of myocardial injury.

Efficacy of spectral presaturation of inversion recovery in evaluating delayed myocardial enhancement.

OBJECTIVE: Delayed myocardial enhancement is caused by a variety of cardiovascular diseases. The extent of the enhanced area has been examined by the inversion recovery (IR) method, whereby at the inversion time (TI), normal myocardium shows a low signal intensity. In this sequence, as pericardial fat shows a very high intensity, a delayed enhancement just below the pericardium may be indistinct. To improve the accuracy of delayed myocardial enhancement, we employed the spectral presaturation of inversion recovery (SPIR) method. MATERIALS AND METHODS: Thirty-five patients with symptoms of cardiovascular disease aged between 36 and 80 years old (mean age, 62 years old) were investigated. Thirty were men and five were women. Inversion recovery and SPIR images were obtained 25 min after initial administration of a gadolinium-based contrast material. Each TI, when the signal intensity of the normal myocardium was null, was determined by images obtained at serial different TIs. A radiologist and a cardiologist examined each image by a consensus reading. The extent of myocardial enhancement was described as none, subendocardial, transmural and a random pattern in each case. Images were ranked over three levels and were based on whether myocardial enhancement could be easily detected or whether the contour of the myocardium was visualized precisely. Student's t-test was conducted to compare the quality of two sequences in all patients and in 22 patients who showed delayed myocardial enhancement. RESULTS: The imaging quality in evaluating delayed myocardial enhancement in all patients was superior with IR compared with SPIR, although it was not statistically significant. The imaging quality in the patients with delayed myocardial enhancement was similar between SPIR and IR. SPIR was superior to the IR sequence in two of the four patients who exhibited transmural enhancement. CONCLUSION: SPIR exhibited equivalent image quality to IR in evaluating delayed myocardial enhancement. As it has the potential advantage in patients with rich adipose tissue surrounding the myocardium, it can be an alternative sequence to evaluate myocardial viability.

Comparison of the effect of the ATP-sensitive potassium channel opener YM934 with that of nitroglycerin on impaired coronary circulation in dogs.

We compared the effect of an ATP-sensitive potassium channel opener, YM934, with that of nitroglycerin (NTG) on impaired coronary circulation in dogs. Coronary stenosis was produced in 7 dogs by placing a hydraulic occluder around the proximal left circumflex coronary (LCx) artery and abolishing reactive hyperemia to compromise the LCx flow. The following parameters were measured: the aortic pressure, LCx flow velocity, LCx vessel diameter, LCx peripheral pressure, and segment length in the LCx area. Subsequently, we occluded the LCx artery for 15 seconds and measured the recovery-interval (time required for the segment shortening to return to the preocclusion value). The measurements were recorded under three study conditions: (1) at baseline without LCx stenosis; (2) with LCx stenosis under NTG infusion (3 microg/Kg/min); and (3) with LCx stenosis after intravenous administration of YM934 (0.3 microg/kg). The heart rate and aortic pressure were similar under the three study conditions. Mean LCx flow velocity and segment shortening did not significantly change either. However, LCx peripheral pressure decreased after the induction of stenosis (P < 0.05) and showed no response to either NTG or YM934. YM934 administration significantly increased LCx flow in the presence of LCx stenosis, (P < 0.05), whereas NTG infusion did not. YM934 significantly shortened the recovery-interval of the segment shortening after 15-sec LCx occlusion (P < 0.05), whereas NTG did not. These findings suggest that YM934 improves coronary blood flow and prevents myocardial ischemic damage in severely impaired coronary circulation.

[Magnesium in congestive heart failure].

Magnesium deficit and other electrolyte abnormalities is a frequent disorder in patients with congestive heart failure. Overstimulation of the renin-angiotensin-aldosterone system, long-term administration of diuretics, digoxin, poor oral intake and impaired absorption contribute to these electrolytes abnormalities. Hypomagnesaemia and depletion of intracellular magnesium stores have been held responsible for a variety of cardiovascular and other functional abnormalities, including various arrhythmias, impairment of cardiac contractility, and vasoconstriction. Because sudden death is prevalent in congestive heart failure, a causal relationship between arrhythmias and magnesium deficiency has been proposed. Reportedly, administration of magnesium can suppress ventricular arrhythmias;however, it remains to be elucidated whether administration of magnesium prevents sudden death and improves prognosis of the patients with congestive heart failure. Nevertheless, since magnesium depletion may be prevalent in congestive heart failure and magnesium has anti-arrhythmic and beneficial cardiovascular effects, magnesium should be supplemented to the patients suspected to have its deficiency.

A porcine model of ischemic heart failure produced by chronic placement of a tube in a coronary artery.

BACKGROUND AND AIMS: Animal models of heart failure (HF) are useful to clarify the mechanism and to develop therapeutic interventions. To produce an easy ischemic HF model, we induced myocardial infarction (MI) in pigs by placing a tube in the coronary artery. METHODS: Twelve pigs underwent echocardiography and were randomly allocated to the myocardial infarction group (MI group) and the control group. In the MI pigs, a 4.2 F nylon tube was placed via the carotid artery in the left circumflex coronary (LCx) artery to induce MI. Three months thereafter, thoracotomy was performed in the both groups and left ventricular (LV) pressure-volume relation was evaluated. RESULTS: Body weight, LV dimension and function did not differ in the baseline state between the two groups. Three months after the tube placement, LV diameter was larger (47+/-3 vs. 42+/-2 mm) and its fractional shortening was lower in the MI group than the control group. In addition, aortic flow was decreased, LV ejection fraction was decreased (25+/-5 vs. 52+/-6%) and LV diastolic pressure was elevated (14+/-3 vs. 8+/-2 mmHg) in the MI group compared with the control group. The extent of MI was 26+/-5% of the LV in the MI pigs. CONCLUSION: The method of placing a tube in the coronary artery does not need thoracotomy or an additional procedure and enables the production of an ischemic HF model of pigs.

Amlodipine improves vascular function in patients with moderate to severe hypertension.

The long-term effects of amlodipine, a calcium channel blocker, were examined in patients with moderate to severe hypertension. Eighteen never-treated patients with moderate to severe essential hypertension (49 +/- 8 years) were studied. In all patients, forearm blood flow (FBF) was measured by plethysmography before and 6 months after amlodipine treatment. Endothelium-nondependent and endothelium-dependent vasodilations were assessed by intrabrachial infusion of sodium nitroprusside (SNP) and acetylcholine (ACh), respectively. FBF modification by vitamin C, an oxygen radical scavenger, was also assessed under ACh infusion. The results were compared with those of 13 normal subjects. Blood pressure was significantly lowered (from 176 +/- 17/97 +/- 13 to 144 +/- 12/82 +/- 10 mm Hg) after treatment (P < 0.01). Forearm vascular resistance was increased in the hypertensive patients before treatment; however, it was normalized after treatment during SNP infusion and was improved during ACh infusion. Since vitamin C improved FBF under ACh infusion both before and after the amlodipine treatment, it is suggested that the production of free radicals was not canceled by amlodipine. The analysis of heart rate variability showed that amlodipine does not activate sympathetic nerve function. Therefore, amlodipine is effective in lowering blood pressure associated with the improvement of vascular function, and is suggested to be an effective antihypertensive agent for patients with moderate to severe hypertension.

Effects of nicardipine on coronary, vertebral and renal arterial flows in patients with essential hypertension.

We examined the acute effects of a calcium antagonist, nicardipine, on hemodynamics and blood flow in the left anterior descending coronary (LAD), vertebral and renal arteries of essential hypertensive patients who had complained of chest pain and undergone cardiac catheterization. The blood flow velocities of the LAD, vertebral and renal arteries were measured using a Doppler guidewire and the arterial luminal diameters were measured from the arteriograms. The arterial blood flow was calculated by multiplying the blood flow velocity by the obtained vessel diameter. Coronary flow reserve was evaluated by injecting papaverine into the left coronary artery. After the baseline data had been obtained, intravenous infusion of nicardipine was started and the same hemodynamic, blood flow velocity and arterial diameter measurements were repeated. Blood pressure was decreased and cardiac output was increased by nicardipine infusion. There was a correlation between the decrease in systolic blood pressure and the increase in cardiac output (r = 0.71). The blood flow velocity in the LAD, vertebral and renal arteries tended to increase and there was an increase in the arterial luminal diameter. An increase in blood flow and a lowering of vascular resistance were observed for each artery (p < 0.05). During nicardipine infusion, the diastolic blood flow in the LAD artery was improved (p < 0.05); however, the maximal blood flow in the LAD artery induced by papaverine infusion remained unchanged. Therefore, there is evidence that coronary, vertebral and renal blood flows are improved by nicardipine infusion despite the acute blood pressure reduction.

Peripartum cardiomyopathy and biventricular thrombi.

Peripartum cardiomyopathy is a rare cardiac disorder characterized by the development of heart failure in the last month of pregnancy or up to 5 months postpartum in women without other determinable causes of cardiac failure. Intracardiac thrombi have been found at autopsy in some patients with this condition and have been demonstrated in the left or right ventricles on 2-dimensional echocardiography. A 23-year-old woman presented with peripartum cardiomyopathy and biventricular thrombi on echocardiography. The thrombi were spherical, pedunculate, shaggy and irregular in configuration, and freely mobile, suggesting that they were fresh. She was treated with conventional heart failure therapy and anticoagulants. Four days later, the apical thrombi within both ventricles had disappeared and there was no evidence of embolism on physical examination. The hypercoagulable state of the peripartum period and the severe biventricular dysfunction most likely led to the formation of biventricular thrombi.

Effects of anti-vasospastic agents in Japanese patients with dilated cardiomyopathy and coronary vasospasm.

The pathogenesis of dilated cardiomyopathy (DCM) is unknown, but clinical evidence suggests that coronary vasospasm is associated with the development of DCM in some cases. In the present study, we aimed to clarify the prevalence of coronary vasospasm in patients with DCM, the characteristics of patients with DCM and coronary vasospasm, and the effects of anti-vasospastic agents on patients with DCM and coronary vasospasm. This study included 18 consecutive patients with DCM who underwent cardiac catheterization with ergonovine provocation testing. The patient was diagnosed as having coronary vasospasm if ergonovine induced coronary vasoconstriction > or = 75% diameter narrowing was observed compared to the diameter after nitroglycerin administration. Six (33%) patients were found to have coronary vasospasm and anti-vasospastic agents were added after the cardiac catheterization. The prevalence of atrial fibrillation in the patients with DCM and coronary vasospasm was greater than that in DCM without coronary vasospasm [67% vs 8% (P<0.05)]. The left ventricular end-diastolic dimension decreased from 61 mm (56/64) to 55 mm (53/56) (median, 25th/75th percentile, P<0.05) and the left ventricular ejection fraction increased from 36% (32/40) to 47% (46/48) (median, 25th/ 75th percentile, P<0.05) after the administration of anti-vasospastic agents and 4 of the 6 patients improved symptomatically. Therefore, ergonovine provocation testing is useful in identifying patients with DCM and coronary vasospasm, in whom cardiac performance is expected to be improved with anti-vasospastic agent therapy. DCM patients with atrial fibrillation may be a clue for identifying patients with coronary vasospasm.

Magnesium sulphate infusion suppresses the cardiac release of noradrenaline during a handgrip stress test.

BACKGROUND: Magnesium has several important cardiovascular effects, but its effect on cardiac sympathetic efferent neuron activity has not been clarified. OBJECTIVES: To examine the effect of magnesium sulphate infusion on cardiac sympathetic efferent postganglionic neuronal liberation of noradrenaline. PATIENTS AND METHODS: Twenty-two patients who underwent cardiac catheterization were randomly allocated to the control group or the magnesium group. Plasma noradrenaline and adrenaline concentrations in the aorta and the coronary sinus were measured. Noradrenaline or adrenaline release from the heart was calculated by dividing the difference in noradrenaline or adrenaline concentration between the aorta and the coronary sinus by that of the aorta. After baseline blood sampling, the control patients and the patients in the magnesium group received intravenous infusion of saline or magnesium sulphate (10 mmol). All patients were then subjected to 3 min of handgrip exercise stress test to augment sympathetic efferent neuronal activity, and the blood sampling was repeated. RESULTS: Although blood pressure was increased by the handgrip stress test, there were no differences in heart rate and blood pressure between the two groups, both at baseline and during the handgrip stress test. The plasma noradrenaline and adrenaline concentrations and noradrenaline or adrenaline release from the heart did not differ between the two groups in the baseline condition. However, the handgrip stress increased plasma noradrenaline concentrations and the cardiac noradrenaline release was increased in the control group, whereas the cardiac noradrenaline release was not increased by the handgrip stress in the magnesium group (P<0.02). CONCLUSIONS: These data indicate that magnesium sulphate infusion suppresses the release of catecholamines by the heart, which is an indirect index of sympathetic efferent neuronal activity.