Acute myocardial infarction caused by a septic coronary embolism diagnosed and treated with a thrombectomy catheter.

Acute myocardial infarctions are common in bacteraemia but are seldom diagnosed during life. A 64 year old man with severe chest pain who had fever for several days due to possible bacteraemia was shown by ECG and echocardiography to have possible lateral infarction. Immediate coronary angiography showed possible thrombus in the left circumflex artery, which was treated by thrombectomy catheter. Bacterial thrombus was removed and was verified by histological examination. A stent was implanted without complications. Acute myocardial infarction caused by septic embolism is usually fatal; however, thrombectomy may be useful in these cases.

Relationship between evaluation by quantitative fatty acid myocardial scintigraphy and response to beta-blockade therapy in patients with dilated cardiomyopathy.

Predicting the effect of beta-blockade therapy on the clinical outcome of patients with dilated cardiomyopathy (DCM) is difficult prior to the initiation of therapy. Myocardial fatty acid metabolism has been shown to be impaired in patients with DCM. We examined whether the extent of myocardial injury, as assessed by iodine-123 15-( p-iodophenyl)-3- R, S-methylpentadecanoic acid (BMIPP) myocardial scintigraphy, is related to the response of patients with DCM to beta-blockade therapy. Thirty-seven patients with DCM were examined using BMIPP myocardial scintigraphy before and after 6 months of treatment with metoprolol. Myocardial BMIPP uptake (%BM uptake) was estimated quantitatively as a percentage of the total injected count ratio. The left ventricular end-diastolic and end-systolic dimensions (LVDd, LVDs) and ejection fraction (LVEF) were also evaluated. The patients were divided into two groups according to their functional improvement (>10% elevation of LVEF) after 6 months of metoprolol therapy. Twenty-eight patients responded to the therapy, while nine did not. Prior to the therapy, no significant differences in LVDd, LVDs or LVEF were observed between the responders and non-responders. However, the %BM uptake was significantly lower in the non-responders than in the responders (1.0%+/-0.2% vs 2.1%+/-0.5%, P<0.001). The %BM uptake could be used to distinguish the responders from the non-responders with a sensitivity of 0.93 and a specificity of 1.00 at a threshold value of 1.4. After the metoprolol therapy, the %BM uptake improved significantly in the responders (2.5%+/-0.5%, P<0.01) but did not change in the non-responders. These results indicate that myocardial BMIPP uptake could predict the response of DCM patients to beta-blockade therapy.

Circadian variation of the onset of acute myocardial infarction in the Osaka area, 1998-1999: characterization of morning and nighttime peaks.

The onset of acute myocardial infarction (AMI) shows characteristic circadian variations; that is, a definite morning peak related to biologic rhythms and a vague nighttime peak related to socioeconomic factors. The recent economic recession in Japan may change the circadian variation, especially the nighttime peak. This study evaluated the recent circadian variation of AMI in Osaka and specified the patient subgroups showing either a morning or nighttime peak predominantly. Of 1,609 consecutive patients with AMI registered from April 1998 to January 2000, 1,252 whose onset of AMI was definitely identified were studied. The day was divided into six 4-h periods with a morning peak between 08.01 h and 12.00h, and nighttime peak between 20.01 h and 24.00h. When subgroup analysis was performed, female patients aged 65 years or more showed a morning peak alone and male patients aged less than 65 years with an occupation and the habits of cigarette smoking and alcohol intake showed a nighttime peak alone. Thus, in Osaka nighttime socioeconomic factors may currently be more potent triggers of AMI than the morning surges in younger male workers who smoke and drink.

Increased angiotensin-converting enzyme activity in coronary artery specimens from patients with acute coronary syndrome.

BACKGROUND: Angiotensin-converting enzyme (ACE) inhibitors are effective in the secondary prevention of ischemic heart disease, but they do not reduce the rate of restenosis. Vascular ACE activity in the culprit coronary lesions of these patients, however, has never been quantified. METHODS AND RESULTS: We measured the ACE activity of vascular tissue obtained by directional coronary atherectomy in patients with acute coronary syndrome (n=17) and in patients with stable ischemic heart disease (n=36), with and without restenosis. The ACE activity of the culprit coronary lesions was significantly increased in patients with acute coronary syndrome (0.87+/-0.12 nmol. min(-1). mg protein(-1); P:<0.01) but not in patients with ischemic heart disease with restenosis (n=11, 0.19+/-0.05 nmol. min(-1). mg protein(-1)) when compared with those patients with ischemic heart disease without restenosis (n=25, 0.20+/-0.05 nmol. min(-1). mg protein(-1)). There was no difference between the ACE activity of the coronary tissue of the in-stent (n=5) and stent-unrelated (n=6) restenosis patients (0.24+/-0.10 versus 0.15+/-0.04 nmol. min(-1). mg protein(-1)). Serum ACE activity did not differ significantly among the patients. CONCLUSIONS: The present study demonstrates increased ACE activity in culprit lesions in acute coronary syndrome, indicating that enhanced ACE activity is related to the causative mechanism of active coronary lesions.

Time to recover from atrial hormonal, mechanical, and electrical dysfunction after successful electrical cardioversion of persistent atrial fibrillation.

Although transient atrial dysfunction has been reported after electrical cardioversion of atrial fibrillation (AF), the difference in the time to recover from the atrial hormonal, mechanical, and electrical dysfunction has not been described. Thus, we evaluated the time course of recovery from atrial hormonal, mechanical, and electrical dysfunction after cardioversion in patients with nonvalvular AF. We attempted electrical cardioversion in 87 consecutive patients with nonvalvular AF that had persisted for > or =6 months, and in 24 patients (28%) with maintained sinus rhythm for > or =6 months. To evaluate atrial hormonal, mechanical, and electrical dysfunction in these 24 patients, we measured plasma concentration of atrial natriuretic peptide, the atrial peak velocity in transmitral flow, and the ratio of peak systolic-to-diastolic pulmonary venous flow (S/D ratio) using echocardiography, and the duration and the root mean voltage for the terminal 20 ms (LP20) of the filtered P wave using P-wave signal-averaged electrocardiography. Atrial natriuretic peptide rapidly returned to baseline within 1 day after cardioversion, and maintained these levels for 6 months. Atrial peak velocity in transmitral flow and S/D ratio were significantly increased at 2 weeks, and continued to increase until 1 month, and then reached a plateau. The duration and LP20 began to recover only 6 months after cardioversion. One to 3 years after conversion, the duration and LP20 had nearly reached a plateau, but the latter value remained below normal. In patients with nonvalvular AF of prolonged duration, recovery from atrial electrical dysfunction after sinus conversion took much longer than that from either atrial hormonal or mechanical dysfunction.

Evaluation of contrast agents for delineation of vessel wall boundary by intracoronary ultrasound after coronary angioplasty in human.

We evaluated the potential for improving visualization at intervention sites using contrast-enhanced intracoronary ultrasound (ICUS) and the suitable contrast agents for this procedure in humans. In 37 patients, ICUS (30 MHz) was performed with intracoronary bolus injection (3 mL) of seven different contrast preparations and without the contrast agents (control) after coronary intervention. The contrast agents used were as follows: saline solution, standard iomeprol, standard ioxaglate, sonicated iomeprol, sonicated ioxaglate, 50% Albunex, and 100% Albunex. Homogeneous and complete opacification of the vessel lumen and false lumen was observed with sonicated ioxaglate, 50% and 100% Albunex. Shadowing was not observed at all with sonicated ioxaglate and was uncommon with 50% Albunex, whereas 100% Albunex caused shadowing in all cases. The coronary delineation rate with the other contrast agents was only 60%-70%, and the homogeneity and peak intensity were relatively low. Thus, sonicated ioxaglate and 50% Albunex both achieved good visualization, but the latter is more expensive, more difficult to handle, and takes longer to prepare. Of the agents we studied, sonicated ioxaglate appears to be best suited for contrast-enhanced ICUS. ICUS using suitable contrast agents could only visualize the large dissections and the strategy was changed according to the contrast-enhanced ICUS results in five cases. Thus, suitable contrast agents, e.g., sonicated ioxaglate, should be used during ICUS after intracoronary intervention.

Dobutamine stress echocardiography at 7.5 mg/kg/min using color tissue Doppler imaging M-mode safely predicts reversible dysfunction early after reperfusion in patients with acute myocardial infarction.

Dobutamine stress echocardiography (DSE) is widely used to predict reversible left ventricular dysfunction, but evaluation by this method is subjective. The recently developed color tissue Doppler imaging (TDI) M-mode may permit objective and quantitative assessment of changes in wall motion induced by DSE. We tested the hypothesis that this new method can detect sensitively reversible dysfunction in the post-myocardial infarction setting. DSE with color TDI M-mode and conventional DSE were performed to predict reversible dysfunction in 53 patients at a mean of 3 days after infarction using 7.5 and 10 microg/kg/min of dobutamine. Follow-up regular echocardiography (4 weeks later) was used as the reference technique to define reversible dysfunction segments. To predict reversible dysfunction segments, the standard segmental wall motion score change on conventional DSE and the ratio of the segmental wall velocity difference at rest versus stress (7.5 and 10 microg/kg/ min) on DSE with color TDI M-mode (7.5-TDI-M and 10-TDI-M, respectively) were used. With 7.5 microg/kg/min of dobutamine, the sensitivity for predicting reversible dysfunction using color TDI M-mode (7.5-TDI-M) was significantly higher than that of conventional DSE (89% vs 73%, p <0.05) whereas specificities and predictive values were almost identical. With a 10-microg/kg/min dose, color TDI-M mode (10-TDI-M) and conventional DSE were not significantly different in predicting reversible dysfunction. With use of color TDI-M mode, regional wall motion during DSE was analyzed objectively and quantitatively. Moreover, combined TDI-M and conventional data were slightly superior to either mode alone. There were no arrhythmias during 7.5 microg/kg/min of dobutamine, but 9 arrhythmias occurred during the 10-microg/kg/min dose in patients with acute myocardial infarction. In conclusion, color TDI M-mode permits objective and quantitative assessment of regional ventricular wall motion and gives additional information for detecting reversible dysfunction in DSE. Improvement of sensitivity at a lower dose of dobutamine with color TDI-M mode may increase the safety of DSE in the post-myocardial infarction setting.

[Clinical usefulness of contrast-enhanced intracoronary ultrasound (ICUS) and evaluation of suitable contrast agents for ICUS].

It is sometimes difficult to visualize the luminal borders of the vessel even by intracoronary ultrasound (ICUS), especially after coronary intervention. In this study, we evaluated the potential for improving visualization at intervention sites using contrast-enhanced ICUS and the suitable contrast agents for this procedure in humans. In 37 patients, ICUS (30 MHz) was performed with intracoronary injection (3 ml) of 7 different contrast preparations and without the contrast agents (control) after coronary intervention. The contrast agents used were as follows: saline solution, standard iomeprol, standard ioxaglate, sonicated iomeprol, sonicated ioxaglate, 50% Albunex, and 100% Albunex. Vessel wall delineation, contrast homogeneity (Grade 0-3), peak contrast intensity and shadowing were examined. Homogeneous and complete opacification of the vessel lumen and false lumen was observed with sonicated ioxaglate, 50% and 100% Albunex. Shadowing was not observed at all with sonicated ioxaglate and was uncommon with 50% Albunex, whereas 100% Albunex caused shadowing in all cases. The coronary delineation rate with the other contrast agents was only 50-70 %, and the homogeneity and peak intensity were relatively low. Thus, sonicated ioxaglate and 50 % Albunex both achieved good visualization, but the former is cheaper, stable and takes shorter to prepare. Large dissection in 5 patients were found by contrast-enhanced ICUS' whereas they were not detected by coronary angiography. All of them needed additional interventional therapy due to the results of contrast-enhanced ICUS. In conclusion, contrast-enhanced ICUS is useful for evaluation of the results by intervention therapy, and of the agents we studied sonicated ioxaglate is best for contrast-enhanced ICUS.

Prethrombotic state due to hypercoagulability in patients with permanent transvenous pacemakers.

Venous thrombosis is a relatively usual but serious complication of permanent transvenous pacing. However, the pathogenesis has not been defined. To clarify underlying abnormalities in the coagulation-fibrinolysis system in patients with permanent transvenous pacemakers, we measured serum levels of fibrinopeptide A (FPA), thrombin-antithrombin III complexes (TATs), plasmin-alpha 2 plasmin inhibitor complexes (PICs), D-dimer (D-D), beta-thromboglobulin (beta-TG), and platelet factor 4 (PF4) in 53 patients with permanent transvenous pacemakers and 10 control subjects. The patients were divided into two groups, as follows, according to the presence of mural thrombus documented along the pacing lead(s) by digital subtraction angiography and transesophageal echocardiography: Group Th (-), patients without venous route thrombus; and Group Th (+), patients with venous route thrombus. FPA and TAT levels increased significantly even in Group Th (-), and further increased in Group Th (+) compared with control subjects (FPA: 7.5 +/- 4.9, 15.3 +/- 8.8 vs 3.0 +/- 1.4 ng/mL, respectively, P < 0.05; TAT: 2.9 +/- 1.3, 4.8 +/- 2.3 vs 1.7 +/- 0.6 ng/mL, respectively, P < 0.05). There were no differences in levels of D-D, PIG, beta-TG, and PF4 among control subjects, Group Th (-), and Group Th (+). These findings suggest that the hypercoagulable state appears in patients with permanent transvenous pacemakers, even without apparent venous thrombosis. The patients with permanent transvenous pacemakers are thought to be in the prethrombotic state even if they have no venous route thrombosis.

Echographic detection of latent severe thrombotic stenosis of the superior vena cava and innominate vein in patients with a pacemaker: integrated diagnosis using sonography, pulse Doppler, and color flow.

Thrombosis of the innominate vein and SVC is a serious complication in patients with pacemakers, inducing pulmonary embolism or SVC syndrome. Venography is the definitive method for its diagnosis; however, it is too invasive for related studies. The purpose of this study was to validate sonography, pulse Doppler, and color flow in detecting noninvasively innominate vein or SVC thrombosis in patients with pacemakers. In 53 patients with pacemakers, the 1 severe SVC stenosis and 18 severe innominate vein stenoses due to thrombosis were diagnosed by digital subtraction angiography. Sonography accurately showed the severe SVC stenosis due to thrombosis, but had limitations on the innominate vein thrombosis. Color flow demonstrated mosaic flow, indicating poststenotic turbulence due to stenosis of the innominate vein and SVC caused by thrombosis in 15 of 16 patients, and pulse Doppler disclosed absence of flow due to complete occlusion of the innominate vein in 2 of 2 patients. Sensitivity and specificity for detecting severe innominate vein stenosis due to thrombosis using combined color flow and pulse Doppler was 94% and 100%, respectively. In conclusion, sonography, pulse Doppler, and color flow allow accurate detection of severe innominate vein or SVC stenosis due to thrombosis, and are therefore useful for the follow-up of patients with a pacemaker.

Superior vena cava syndrome due to a permanent transvenous pacing lead.

Superior vena cava (SVC) syndrome after pacemaker implantation is a very rare complication. We present a 56-year-old man with severe swelling of the face, neck, and upper arms about 6 years after pacemaker implantation. Digital subtraction angiography showed occlusion of the left innominate vein and severe stenosis of the SVC. The patient eventually required surgical treatment, since anticoagulant therapy and balloon venoplasty were not effective. We conclude that surgical repair is the most effective method for treating similar patients.

Recovery of impaired left ventricular function in patients with acute myocardial infarction is predicted by the discordance in defect size on 123I-BMIPP and 201Tl SPET images.

A discrepancy between myocardial perfusion defect and wall motion abnormalities is frequently found early after coronary reperfusion in patients with acute myocardial infarction. The purpose of this study was to assess recovery of impaired left ventricular function by reference to the discordance in defect size between myocardial fatty acid uptake and myocardial perfusion using combined single-photon emission tomographic (SPET) imaging early after coronary perfusion therapy. In 37 patients with acute myocardial infarction, iodine-123 15-(p-iodophenyl)-3(R, S)-methylpentadecanoic acid (BMIPP) and thallium-201 SPET scans were performed early after coronary reperfusion. A severity score was determined from the extent of the imaging defect with each tracer. Left ventricular wall motion score (WMS) and ejection fraction (EF) were obtained at admission and at 4 weeks after the onset of infarction. In 32 of the 37 patients, discordance in defect sizes delineated with the two SPET studies was found during the acute stage. The severity score for BMIPP was larger than that for 201Tl during the acute stage (7. 7+/-2.4 vs 4.4+/-2.5, P <0.001). There was a fair correlation between the severity score for BMIPP and WMS (r=0.82, P <0.0001), but a poor correlation between that for 201Tl and WMS. The extent of discordance in severity scores between BMIPP and 201Tl during the acute stage correlated well with the extent of the improvement in WMS (r=0.86, P <0.0001) and that of EF (r=0.85, P <0.0001). We conclude that the discordance in defect size on BMIPP and 201Tl SPET images during the acute stage of infarction is an early predictor of the viability of the myocardium at risk of infarction.

Non-ischemic myocardial fibrosis after long-term asbestos exposure.

To determine whether or not myocardial fibrosis in the left ventricle increases after exposure to asbestos fiber, we studied myocardial fibrosis in 42 autopsied hearts; 17 of asbestosis (AS) and 18 of chronic pulmonary disease (CP) without pneumoconiosis. Seven patients with extracardiopulmonary disease were used as a control group (CONT). The extent of myocardial fibrosis in the left ventricle was significantly greater in the AS group compared to the other groups (AS 3.6 +/- 1.3% vs. CP 2.4 +/- 1.0% vs. CONT 1.6 +/- 0.8%). There was a significant difference in the appearance ratio of focal fibrosis between the asbestosis group and the other groups. Focal fibrosis was observed in none of 7 control patients, in 3 of 18 patients with chronic pulmonary disease and in 9 of 17 patients with asbestosis. We concluded that characteristic myocardial fibrosis was observed in humans after long-term asbestos exposure.

Endothelial dysfunction in the early stage of atherosclerosis precedes appearance of intimal lesions assessable with intravascular ultrasound.

The objective of this study was to clarify whether morphologic evaluation of the in vivo artery with intravascular ultrasound provides as sensitive a marker as endothelial dysfunction or microscopic histologic assessment. Endothelial dysfunction assessed with the changes in the vessel diameter during acetylcholine infusion has been used as a more sensitive marker of atherosclerosis than the angiographic estimates of morphologic structure of the vessel. Recent advent of intravascular ultrasound has provided such high-resolution images of the vessels that morphologic changes in the vessel structure are sensitively and accurately detected. Twenty-two rabbits were divided into three groups: six rabbits fed a cholesterol-rich diet for 2 weeks as the hypercholesterolemia group, eight rabbits fed with the diet for 8 weeks as the atherosclerosis group, and eight rabbits fed a normal diet as the normal group. After evaluating the atherosclerotic lesions by intravascular ultrasound, the cross-sectional area was measured in the baseline and during the infusion of acetylcholine (0.05, 0.5, and 5 micrograms/kg/min) and nitroglycerin (5 micrograms/kg/min). No atherosclerotic lesions were detectable with intravascular ultrasound in any rabbit despite the presence of microscopic intimal lesions in the vessels in the rabbits of the atherosclerosis group. The cross-sectional area increased during acetylcholine infusion in the rabbits of the normal and the hypercholesterolemia groups. In contrast, in the rabbits of the atherosclerosis group, the cross-sectional area did not significantly increase during acetylcholine infusion at the rate of 0.5 microgram/kg/min and even tended to decrease at the rate of 5 micrograms/kg/min (-3.8% +/- 3.7%, P < 0.05 vs the normal group). Dilating responses to nitroglycerin infusion were similar among all three groups. In conclusion, impairment of the endothelium-dependent vasodilating response assessed with intravascular ultrasound in the in vivo vessel precedes the appearance of echographic atherosclerotic findings. Thus intravascular ultrasound, if used in combination with drug intervention to assess endothelial function, would provide even more accurate assessment of the vessels than conventional intravascular ultrasound alone.

Transesophageal echocardiographic diagnosis of thoracic aortic dissection with the completely thrombosed false lumen: differentiation from true aortic aneurysm with mural thrombus.

The conventional criteria of aortic dissection with a completely thrombosed false lumen by transesophageal echocardiography is separation of the intima from the layer of thrombus; however, it is not always easy to distinguish from true aortic aneurysm with mural thrombus. Thus we proposed a new transesophageal echocardiographic diagnostic criteria. Seventeen operative patients with suspected subacute or chronic thoracic aortic dissection in whom it was difficult to exclude true aortic aneurysm with mural thrombus underwent transesophageal echocardiography. In thoracic aortic dissection with in completely thrombosed false lumen, the inner lesion surface composed of intima may be smooth and crescent-shaped thrombus may appear inside the wall surface. Therefore our criteria were on the basis of any two of the following: (1) high-echogenic lesion surface, suggesting intima, over the thrombus, (2) smooth lesion surface, and (3) crescent-shaped thrombus. Imaging data were referenced to intraoperative findings. According to the present criteria only two out of 17 patients were misdiagnosed, whereas according to the conventional criteria six patients were misdiagnosed. The sensitivity was significantly higher than when the conventional criteria were used (90% versus 40%; p < 0.05), whereas the specificity was similar. We conclude that the present transesophageal echocardiographic criteria for detection of thoracic aortic dissection with a completely thrombosed false lumen is clinically useful.

Basal release of endothelium-derived nitric oxide plays an important role in the prevention of afterload mismatch in acute left ventricular dysfunction.

The basal release of endothelium-derived nitric oxide (EDNO) is considered to play an important role in regulating the vascular tone in normal subjects; however, its role in the presence of acute heart failure is unknown. This study was designed to clarify the role of a basal release of EDNO in the presence of acute heart failure. Acute ischemic left ventricular (LV) dysfunction was produced in 22 dogs by coronary microembolization. After the embolization, only saline solution was intravenously infused for sixty minutes in 10 dogs. In another 12 dogs, NG-monomethyl-L-arginine (L-NMMA), which is known to inhibit the formation of EDNO in the vascular endothelium, was intravenously infused at a rate of 20 micrograms/kg/minute for sixty minutes. Infusion of saline solution did not produce any changes in hemodynamic variables. Infusion of L-NMMA caused increases in mean aortic pressure, systemic vascular resistance, and LV end-diastolic pressure without changes in the LV peak + and - dP/dt (time constant) of LV pressure fall, and these changes were associated with a giant "v" wave in the tracing of left atrial pressure and a decrease in cardiac output. The basal release of EDNO may play an important role in the prevention of afterload elevation, subsequent cardiac output reduction, and afterload mismatch in the presence of acute heart failure.

Transesophageal echocardiography combined with magnetic resonance imaging for detecting venous anomalies in dextrocardia. A case report.

A fifty-six-year-old woman was admitted to Osaka Rosai hospital because of dyspnea, chills, and fatigue. The patient was diagnosed by transthoracic echocardiography as having congestive heart failure due to severe biatrioventricular valve regurgitation, and cardiac surgery was proposed. Preoperative transesophageal echocardiography (TEE) revealed a dilatation of the coronary sinus (CS), a right-sided hemiazygos vein (R-AZ), and another great vessel lying between the CS and the R-AZ. Magnetic resonance imaging (MRI) was also performed, and this showed a persistent right superior vena cava (PRSVC) entering the left atrium via the dilatated CS. However, the site of connection between the R-AZ and the PRSVC could not be detected by MRI because of inadequate slice acquisition. Each method has its limitations, particularly with regard to visualizing the extracardiac vascular system. Therefore, the authors demonstrated that the combination of TEE and MRI might be more useful than each alone, and the combination is as a valuable method as digital subtraction angiography for the diagnosis of extracardiac venous anomalies.

Intraventricular dispersion of early diastolic filling: a new marker of left ventricular diastolic dysfunction.

Mitral flow velocity patterns are frequently "normalized" by the alteration in the loading condition even in the presence of left ventricular (LV) diastolic dysfunction. In addition, a simple index, the ratio of mitral peak early diastolic flow velocity to mitral peak flow velocity at atrial contraction, is not obtainable in patients with atrial fibrillation (Af). Thus these limitations hamper the value of analyzing the mitral flow velocity pattern in the assessment of abnormal LV diastolic characteristics. This study was designed to elucidate the hypothesis that peak early diastolic flow velocity decreases progressively from the base to the apex in patients with LV diastolic dysfunction. Regional diastolic flow velocity patterns at 1, 2, or 3 cm from the mitral tip toward the apex were simultaneously recorded with the mitral flow velocity pattern by using multigate pulsed Doppler echocardiography in 42 subjects with normal LV function (31 normal volunteers and 11 patients with Af only), 17 patients with hypertensive heart disease, and 22 patients with dilated cardiomyopathy. In the normal subjects early diastolic flow velocity at the mitral tip was maintained at the positions 1 to 3 cm away from the tip into the LV cavity. In contrast, regional peak early diastolic flow velocity progressively decreased toward the apex in patients with hypertensive heart disease and dilated cardiomyopathy. These findings were observed even in patients with a normalized mitral flow velocity pattern or those with Af. Thus the assessment of the intraventricular decrease in peak early diastolic flow velocity may be useful in detecting LV diastolic dysfunction, particularly in patients with Af or a "normalized" mitral flow velocity pattern.

Noninvasive assessment of left ventricular relaxation using continuous-wave Doppler aortic regurgitant velocity curve. Its comparative value to the mitral regurgitation method.

BACKGROUND: The most established parameters of left ventricular (LV) relaxation are peak negative value of the first derivative of LV pressure (-dP/dtmax) and the time constant of isovolumic LV pressure fall. The instantaneous pressure gradient between the aorta and the LV during diastole can be calculated from the continuous-wave Doppler aortic regurgitant velocity spectrum. Because the fluctuation of aortic pressure during LV isovolumic relaxation is negligibly minor and because LV minimal pressure is negligibly low, LV pressure during the isovolumic relaxation period may be derived from the continuous-wave Doppler aortic regurgitant velocity spectrum. This study was designed to clarify whether analysis of continuous-wave Doppler aortic regurgitation recording provides accurate measures of LV relaxation over a wide range of LV function and to determine comparative values of aortic and mitral regurgitation methods in the assessment of LV relaxation. METHODS AND RESULTS: In eight mongrel dogs with acute ischemic LV dysfunction, the continuous-wave Doppler aortic regurgitant velocity spectrum was recorded simultaneously with high-fidelity LV and aortic pressures, while the continuous-wave Doppler mitral regurgitant velocity spectrum was recorded simultaneously with high-fidelity left atrial and LV pressures. The aortic regurgitant velocity spectrum was provided for the determination of Doppler-derived mean rate of LV pressure fall in 20 ms after the onset of aortic regurgitation (delta P/delta t-AR) and the time interval from the onset of aortic regurgitation to the point at (1-1/e)1/2 of the maximal aortic regurgitant velocity as an estimate of the time constant. The mitral regurgitant velocity spectrum was provided for Doppler-derived mean rate of LV pressure fall in 20 ms after the point of -dP/dtmax (delta P/delta t-MR) and the time interval from the point of -dP/dtmax to the point with mitral regurgitant velocity of (1/e)1/2 of the mitral regurgitant velocity at the point of -dP/dtmax as an estimate of the time constant. delta P/delta t-AR and delta P/delta t-MR correlated well with catheter-derived -dP/dtmax (r = .92, r = .98, P < .01, respectively). The time constant derived from aortic and mitral regurgitant velocity spectra (tau-AR and tau-MR) also correlated well with catheter-derived time constant (r = .84, r = .76, P < .01, respectively). However, a mean difference of the catheter-derived time constant minus tau-MR was larger than tau-AR (29 +/- 30 versus 4 +/- 17 ms, P < .01, presented as mean +/- 2 SD). CONCLUSIONS: LV relaxation can be assessed from the continuous-wave Doppler aortic regurgitant velocity spectrum. The aortic regurgitation method provides an even more accurate estimate of the time constant compared with the mitral regurgitation method, particularly in the presence of LV dysfunction.

Digital subtraction high-frame-rate echocardiography in detecting delayed onset of regional left ventricular relaxation in ischemic heart disease.

BACKGROUND: Because left ventricular (LV) diastolic function is impaired before systolic function in patients with ischemic heart disease and because ischemic heart disease is constituted of regional rather than global abnormalities of the left ventricle, measures of LV regional diastolic dysfunction, if possible, should provide the most sensitive assessment of the coronary involved region. The objectives of this study are to clarify whether high-frame-rate two-dimensional echocardiography, combined with digital subtraction image processing, may be used to visualize regional LV relaxation abnormalities in patients with ischemic heart disease and to clarify whether this technique provides a measure for the noninvasive assessment of the coronary involved region. METHOD AND RESULTS: In 30 normal subjects and 59 patients with ischemic heart disease, two-dimensional echocardiograms obtained at a rate of 60 frames per second were provided on line for digital subtraction analysis, with which digitized images were continuously subtracted on a frame-by-frame basis. The subtracted images were analyzed to determine the onset of the segmental outward motion of the LV wall in early diastole in each of 16 segments per subject. Regional relaxation index, defined as the interval from the second heart sound to the onset of outward wall motion, was significantly prolonged in the coronary involved segments compared with the normal segments (36.3 +/- 18.0 versus 101.2 +/- 34.0 ms, P < .01). The prolongation in the regional relaxation index was observed even in the coronary involved segments without reduction in systolic wall motion. When a cutoff level of 50.0 ms was used, coronary involved segments could be distinguished from normal or border segments with a sensitivity of 92% and a specificity of 81%. CONCLUSIONS: Digital subtraction high-frame-rate echocardiography may be used to visualize regional LV relaxation abnormalities in patients with ischemic heart disease. The time interval from the second heart sound to the onset of the segmental outward motion of the LV wall (regional relaxation index) obtained with this technique provides a noninvasive and accurate measure for assessing coronary involved regions.