Experiences of Percutaneous Endoscopic Approach for the Mastoid Lesions: A Novel Minimally Invasive Ear Surgery.

OBJECTIVES: We developed a novel keyhole surgery, named "percutaneous endoscopic ear surgery" (PEES), with the aim of further reducing the invasiveness of otologic surgery. We reported the cases we encountered and retrospectively analyzed the invasiveness of PEES. METHODS: We analyzed the ears of eight patients who underwent PEES for mastoid lesions that could not be manipulated with transcanal endoscopic ear surgery (TEES) at our hospital between July 2021 and November 2022. We performed PEES alone in three patients, including one case of type A (preauricular incision) and two cases of type B (retroauricular incision). The last five patients underwent combined endoscopic ear surgery, which is simultaneous PEES and TEES. In these cases, one patient underwent type A PEES, and four patients underwent type B PEES. RESULTS: PEES was performed in all patients without converting to conventional microscopic mastoidectomy. The mean length of skin incisions was 19.1 ± 4.5 mm, which was smaller than that in conventional mastoidectomy. In all cases, the average length of the major axis of the keyhole was <10 mm, indicating that sufficient minimally invasive surgery was achieved. The average depth from the keyhole to the deepest site was 21.6 ± 8.9 mm. There was no change in the mean hearing level before and after the surgery. CONCLUSION: PEES is a minimally invasive procedure for manipulating lesions in the mastoid. In addition, the combination of PEES and TEES is an ideal, minimally invasive procedure that can be used to treat all regions of the temporal bone.

Cervical abscess caused by Mycobacterium tilburgii in a patient carrying anti-interferon gamma autoantibody: A case report and literature review.

Mycobacterium tilburgii, a nonculturable mycobacterium, is an important nontuberculous mycobacterium that occasionally causes serious infections in patients with cellular immune deficiencies. Due to its nonculturable nature, information about its drug susceptibility is not available, and data about its clinical response to antimycobacterial treatment remains insufficient. Here, we report a case of a patient who presented with neck swelling and was finally diagnosed with cervical abscess caused by M. tilburgii carrying anti-interferon gamma autoantibodies using a molecular method. The relevant literature was reviewed in the context of epidemiological and clinical data on M. tilburgii infections. In this report, 15 patients were reported to be infected with M. tilburgii. Almost all patients had a cellular immune deficiency and presented with disseminated infections. Multiple refractory or relapse cases that often required prolonged antimycobacterial treatment have been reported, although a few fatal cases have also been reported. In conclusion, M. tilburgii is an important pathogen in patients with cellular immune deficiency. Physicians should thoroughly investigate cellular immune deficiency, including adult-onset immune deficiency with anti-interferon gamma autoantibodies, in patients with M. tilburgii infection.

Congenital hearing impairment associated with peripheral cochlear nerve dysmyelination in glycosylation-deficient muscular dystrophy.

Hearing loss (HL) is one of the most common sensory impairments and etiologically and genetically heterogeneous disorders in humans. Muscular dystrophies (MDs) are neuromuscular disorders characterized by progressive degeneration of skeletal muscle accompanied by non-muscular symptoms. Aberrant glycosylation of α-dystroglycan causes at least eighteen subtypes of MD, now categorized as MD-dystroglycanopathy (MD-DG), with a wide spectrum of non-muscular symptoms. Despite a growing number of MD-DG subtypes and increasing evidence regarding their molecular pathogeneses, no comprehensive study has investigated sensorineural HL (SNHL) in MD-DG. Here, we found that two mouse models of MD-DG, Largemyd/myd and POMGnT1-KO mice, exhibited congenital, non-progressive, and mild-to-moderate SNHL in auditory brainstem response (ABR) accompanied by extended latency of wave I. Profoundly abnormal myelination was found at the peripheral segment of the cochlear nerve, which is rich in the glycosylated α-dystroglycan-laminin complex and demarcated by "the glial dome." In addition, patients with Fukuyama congenital MD, a type of MD-DG, also had latent SNHL with extended latency of wave I in ABR. Collectively, these findings indicate that hearing impairment associated with impaired Schwann cell-mediated myelination at the peripheral segment of the cochlear nerve is a notable symptom of MD-DG.

Hearing vulnerability after noise exposure in a mouse model of reactive oxygen species overproduction.

Previous studies have convincingly argued that reactive oxygen species (ROS) contribute to the development of several major types of sensorineural hearing loss, such as noise-induced hearing loss (NIHL), drug-induced hearing loss, and age-related hearing loss. However, the underlying molecular mechanisms induced by ROS in these pathologies remain unclear. To resolve this issue, we established an in vivo model of ROS overproduction by generating a transgenic (TG) mouse line expressing the human NADPH oxidase 4 (NOX4, NOX4-TG mice), which is a constitutively active ROS-producing enzyme that does not require stimulation or an activator. Overproduction of ROS was detected at the cochlea of the inner ear in NOX4-TG mice, but they showed normal hearing function under baseline conditions. However, they demonstrated hearing function vulnerability, especially at high-frequency sounds, upon exposure to intense noise, which was accompanied by loss of cochlear outer hair cells (OHCs). The vulnerability to loss of hearing function and OHCs was rescued by treatment with the antioxidant Tempol. Additionally, we found increased protein levels of the heat-shock protein 47 (HSP47) in models using HEK293 cells, including H2 O2 treatment and cells with stable and transient expression of NOX4. Furthermore, the up-regulated levels of Hsp47 were observed in both the cochlea and heart of NOX4-TG mice. Thus, antioxidant therapy is a promising approach for the treatment of NIHL. Hsp47 may be an endogenous antioxidant factor, compensating for the chronic ROS overexposure in vivo, and counteracting ROS-related hearing loss.

Maintenance of stereocilia and apical junctional complexes by Cdc42 in cochlear hair cells.

Cdc42 is a key regulator of dynamic actin organization. However, little is known about how Cdc42-dependent actin regulation influences steady-state actin structures in differentiated epithelia. We employed inner ear hair-cell-specific conditional knockout to analyze the role of Cdc42 in hair cells possessing highly elaborate stable actin protrusions (stereocilia). Hair cells of Atoh1-Cre;Cdc42(flox/flox) mice developed normally but progressively degenerated after maturation, resulting in progressive hearing loss particularly at high frequencies. Cochlear hair cell degeneration was more robust in inner hair cells than in outer hair cells, and began as stereocilia fusion and depletion, accompanied by a thinning and waving circumferential actin belt at apical junctional complexes (AJCs). Adenovirus-encoded GFP-Cdc42 expression in hair cells and fluorescence resonance energy transfer (FRET) imaging of hair cells from transgenic mice expressing a Cdc42-FRET biosensor indicated Cdc42 presence and activation at stereociliary membranes and AJCs in cochlear hair cells. Cdc42-knockdown in MDCK cells produced phenotypes similar to those of Cdc42-deleted hair cells, including abnormal microvilli and disrupted AJCs, and downregulated actin turnover represented by enhanced levels of phosphorylated cofilin. Thus, Cdc42 influenced the maintenance of stable actin structures through elaborate tuning of actin turnover, and maintained function and viability of cochlear hair cells.

Left ventricular systolic dyssynchrony index by three-dimensional echocardiography in patients with decreased left ventricular function: comparison with tissue Doppler echocardiography.

BACKGROUND: Three-dimensional echocardiography (3DE) can simultaneously assess left ventricular (LV) regional systolic motion and global LV mechanical dyssynchrony. METHODS: We used 3DE to measure systolic dyssynchrony index (SDI) (standard deviation of the time from cardiac cycle onset to minimum systolic volume in 17 LV segments) in 100 patients and analyzed the association of SDI with other parameters for LV systolic function or dyssynchrony. Eighteen patients who underwent cardiac resynchronization therapy (CRT) were also evaluated at 6 months after CRT, and the association of baseline SDI and tissue Doppler imaging (TDI) dyssynchrony index (Ts-SD) with the change of LV end-systolic volume (ESV) analyzed. Ts-SD was calculated using the standard deviation of the time from the QRS complex to peak systolic velocity. RESULTS: There was a significant inverse correlation between LVEF and SDI (r =-0.686, P < 0.0001). QRS duration was also significantly correlated to SDI (r = 0.407, P < 0.0001). There was a significant positive correlation between baseline SDI and the decrease in LVESV after CRT (r = 0.42). Baseline SDI was significantly greater in responders (10 patients) than in nonresponders (16.4 ± 5.1 vs. 7.9 ± 2.4%, P < 0.01), but there was no significant difference in Ts-SD. SDI > 11.9% predicted CRT response with a sensitivity of 90% and a specificity of 75%. CONCLUSIONS: SDI derived from 3DE is a useful parameter to assess global LV systolic dyssynchrony and predict responses to CRT.

Left atrial volume predicts adverse cardiac and cerebrovascular events in patients with hypertrophic cardiomyopathy.

AIMS: To prospectively evaluate the relationship between left atrial volume (LAV) and the risk of clinical events in patients with hypertrophic cardiomyopathy (HCM). METHODS: We enrolled a total of 141 HCM patients with sinus rhythm and normal pump function, and 102 patients (73 men; mean age, 61±13 years) who met inclusion criteria were followed for 30.8±10.0 months. The patients were divided into two groups with or without major adverse cardiac and cerebrovascular events (MACCE), a composite of stroke, sudden death, and congestive heart failure. Detailed clinical and echocardiographic data were obtained. RESULTS: MACCE occurred in 24 patients (18 strokes, 4 congestive heart failure and 2 sudden deaths). Maximum LAV, minimum LAV, and LAV index (LAVI) corrected for body surface area (BSA) were significantly greater in patients with MACCE than those without MACCE (maximum LAV: 64.3±25.0 vs. 51.9±16.0 ml, p=0.005; minimum LAV: 33.9±15.1 vs. 26.2±10.9 ml, p=0.008; LAVI: 40.1±15.4 vs. 31.5±8.7 ml/mm2, p=0.0009), while there were no differences in the other echocardiographic parameters.LAV/BSA of ≥40.4 ml/m2 to identify patients with cardiovascular complications with a sensitivity of 73% and a specificity of 88%. CONCLUSION: LAVI may be an effective marker for detecting the risk of MACCE in patients with HCM and normal pump function.

[Congenital ossicular malformation: a study of 27 ears].

Despite otological surgical progress improving clinical congenital ossicular malformation management, some cases remain inadequately treated. We report 27 cases of congenital ossicular malformation, focusing on reasons for remaining or delayed postoperative hearing loss evaluated in 27 congenital ossicular malformation cases in Kyoto Prefecture from 2002 to 2008. Overall success was 93% (25/27) 6 months postoperatively. Two ears had no hearing improvement and three delayed hearing loss 8 to 48 months postoperatively. The first two ears underwent small fenestration stapedotomy with malleus attachment piston, and the other three tympanoplasty type III using an autologous ossicle or total ossicular replacement prosthesis (TORP) as a columella. We discuss problems and solutions using a malleus attachment piston or prosthesis, preoperative audio-and radiological findings, and operative findings including facial nerve anomaly and congenital cholesteatoma.

Fulminant fatal cardiotoxicity following cyclophosphamide therapy.

A 59-year-old male with an abdominal mass that showed a diffuse large B cell lymphoma underwent extirpation of the tumor and chemotherapy. He subsequently received high-dose chemotherapy containing cyclophosphamide (1.5 g/m(2)/day x 2 days), followed by autologous peripheral blood stem cell transplantation. He developed congestive heart failure 5 days after administration of cyclophosphamide. His electrocardiogram showed extremely low voltage with ST segment change and echocardiogram showed diffusely increased left ventricular wall thickness, an increase in myocardial echogenicity, pericardial effusion, and generally decreased systolic function. Congestive heart failure progressed rapidly and he died the following day. Post-mortem examination of the heart revealed myocardial hemorrhage, yellowish brown pericardial effusion, and fibrinous pericarditis. His liver was atrophic and focal necrosis was observed histologically. Cyclophosphamide-induced cardiotoxicity occurred, even though the patient had both shown normal cardiac function before high-dose chemotherapy and had received a lower dose of cyclophosphamide. Concomitant administration of cytarabine might have affected his liver function and there might have been interaction between the drugs.

Intramuscular transplantation of G-CSF-mobilized CD34(+) cells in patients with critical limb ischemia: a phase I/IIa, multicenter, single-blinded, dose-escalation clinical trial.

A number of preclinical studies have indicated the therapeutic potential of endothelial progenitor cells for vascular regeneration in ischemic diseases. A phase I/IIa clinical trial of transplantation of autologous CD34(+) cells, the endothelial and hematopoietic progenitor-enriched fraction, was performed in no-option patients with atherosclerotic peripheral artery disease or Buerger's disease with critical limb ischemia (CLI). CD34(+) cells were isolated from the G-CSF-mobilized apheresis product using a magnetic cell sorting system. CD34(+) cells (10(5)/kg, n = 6; 5 x 10(5)/kg, n = 8; or 10(6)/kg, n = 3) were injected i.m. into the leg with more severe ischemia. The Efficacy Score, representing changes in the toe brachial pressure index (TBPI), Wong-Baker FACES pain rating scale, and total walking distance 12 weeks after cell transplantation, the primary endpoint, was positive, indicating improvement in limb ischemia in all patients, although no significant dose-response relationship was observed. During the 12-week observation after cell therapy, the Wong-Baker FACES pain rating scale, TBPI, transcutaneous partial oxygen pressure, total or pain-free walking distance, and ulcer size serially improved in all patients. No death or major amputation occurred, and severe adverse events were rare, although mild to moderate events relating to G-CSF and leukapheresis were frequent during the 12-week follow-up. In conclusion, the outcomes of this prospective clinical study indicate the safety and feasibility of CD34(+) cell therapy in patients with CLI. Favorable trends in efficacy parameters encourage a randomized and controlled trial in the future.

Detection of severe stenosis and total occlusion in the left anterior descending coronary artery with transthoracic Doppler echocardiography in the emergency room.

BACKGROUND: The noninvasive measurement of coronary flow velocity in the left anterior descending artery (LAD) has recently been realized by using the transthoracic Doppler echocardiography (TTDE). A couple of investigations demonstrated that the diastolic-to-systolic peak velocity ratio (DSVR) by TTDE is a simple and noninvasive method for the detection of severe stenosis in the elective settings. However, the usefulness of DSVR by TTDE in the emergency settings has not been evaluated. OBJECTIVE: The purpose of this study was to assess the clinical feasibility to document the LAD flow by TTDE in emergency patients who complained of chest pain. METHODS: We studied 49 consecutive patients with acute coronary syndrome who were going to undergo emergency coronary angiography (CAG) for the anatomical diagnosis and the facilitated percutaneous coronary intervention (PCI). Prior to CAG, we recorded the LAD flow by TTDE and measured the diastolic peak velocity (DVp), systolic peak velocity (SVp), and their ratio, DSVR (DVp/SVp) of LAD flow. RESULTS: By CAG, the culprit lesions actually resided in the proximal LAD in 36 patients. Among the 36 patients, we detected the Doppler LAD flow in 29. Five out of 7 patients who were unable to detect the LAD flow revealed total occlusions by CAG. DSVR of the LAD is significantly lower in 17 patients who showed severe stenoses (>90%) than those in the rest of 12 patients who did not show such critical stenoses (1.44 +/- 0.16 vs 2.10 +/- 0.26, P < 0.0001). CONCLUSION: In the emergency settings, a noninvasive assessment of the LAD flow by TTDE accurately estimates the critical stenotic lesions of the LAD.

Transthoracic Doppler echocardiographic assessment of left anterior descending coronary artery and intramyocardial artery predicts left ventricular remodeling and wall-motion recovery after acute myocardial infarction.

BACKGROUND: Previous studies reported that a coronary flow velocity (FV) pattern with a rapid diastolic deceleration time (DDT) immediately after percutaneous coronary intervention implies advanced microvascular damage in patients who have experienced an acute myocardial infarction (AMI). METHODS: Using transthoracic echocardiography, we recorded the coronary FV in the left anterior descending coronary artery (LAD) and the FV in the intramyocardial artery 2 days after successful percutaneous coronary intervention in 24 patients who had experienced an anterior AMI. We measured the DDT of the LAD and the intramyocardial artery. DDT of the LAD and the intramyocardial artery was detected in the anteroseptal lesion, the wall motion of which revealed severe hypokinesis or akinesis. We performed echocardiography during both the acute phase and 6 months after the AMI. RESULTS: Patients were divided into two groups (group A: DDT of the LAD < or = 600 milliseconds [n = 10], group B: DDT of the LAD > or = 600 milliseconds [n = 14]). DDT of the LAD and the intramyocardial artery was significantly shorter for group A than group B (373 +/- 223 vs 786 +/- 105 milliseconds, P < .0001). In the acute phase, there were no significant differences in left ventricular (LV) wall-motion score index (WMSI), LV end-diastolic volume (EDV), or ejection fraction (WMSI: 2.38 +/- 0.24 vs 2.08 +/- 0.58, P = .20; LV EDV: 160 +/- 41 vs 154 +/- 34 mL; ejection fraction: 45 +/- 11 vs 46 +/- 5%). However, WMSI and LV EDV in group A were significantly greater than in group B (WMSI: 2.47 +/- 0.16 vs 1.84 +/- 0.57, P = .01; LV EDV: 198 +/- 28 vs 132 +/- 37 mL, P = .0004) and the ejection fraction in group A was significantly lower than in group B (38 +/- 9 vs 55 +/- 10%, P = .001) during the chronic phase. CONCLUSIONS: In patients who had experienced an anterior AMI, we could predict wall-motion recovery of the infarcted area by using the coronary FV of the LAD and FV of the intramyocardial artery.

Reoperation for early failure of a freestyle bioprosthesis using a full root technique.

The case is reported of a 65-year-old male who required reoperation for early failure of a Freestyle stentless valve aortic root bioprosthesis implanted using the full root technique. The bioprosthesis had been implanted to treat annuloaortic ectasia associated with severe aortic regurgitation (AR). At 18 months postoperatively, a new diastolic murmur developed, though without complaint by the patient. Transthoracic echocardiography demonstrated severe AR with aneurysmal dilatation of the non-coronary porcine sinus of Valsalva. Pseudoaneurysm formation, associated with perforation of the non-coronary sinus of Valsalva of the bioprosthesis, was observed at surgery. On inspection, the pseudoaneurysm had pushed the commissures inward, and had created severe aortic valve regurgitation. No infection or calcification was detected on the Freestyle valve, and the aortic root was successfully reconstructed using a composite graft.

Impact of newly diagnosed abnormal glucose tolerance on long-term prognosis in patients with acute myocardial infarction.

BACKGROUND: Newly-diagnosed diabetes mellitus (DM) and impaired glucose tolerance are common among patients with acute myocardial infarction (AMI). However, its significance on long-term clinical outcomes in those patients remains unclear. The present study was designed to determine whether such abnormalities after AMI affect long-term clinical outcomes. METHODS AND RESULTS: Two-hundred and seventy-five AMI patients were prospectively enrolled. Eighty-five had diagnosed DM, while the other 190 did not. According to oral glucose tolerance tests at discharge, non-DM patients were divided into 2 groups: 78 patients with normal glucose tolerance and 112 patients with abnormal glucose tolerance. Patients were followed until they reached the primary endpoint: cardiovascular death or unplanned hospitalization due to major adverse cardiovascular events. The median follow-up period was 5.3 years. Kaplan-Meier survival curves for the abnormal glucose tolerance group were poorer than for normal glucose tolerance, and were equivalent to the pre-diagnosed DM group in prognosis (p<0.0005). Glucometabolic status was the strongest predictor for future cardiovascular events (hazard ratio to normal glucose tolerance; 2.65; confidence interval: 1.37-5.15; p=0.004 in abnormal glucose tolerance and 3.27:1.68-6.38; p=0.0005 in DM). CONCLUSIONS: Abnormal glucose tolerance in patients with AMI is a major risk factor for future cardiovascular events and may critically distinguish high-risk individuals.

[Left ventricular volume and ejection fraction by the axius auto ejection fraction method: comparison with manual trace method and visual assessment of ejection fraction].

OBJECTIVES: Visual assessment of the ejection fraction (EF) is often used in clinical practice, but is subjective and requires training and experience. The auto EF method has been newly developed for automated detection of the left ventricular (LV) endocardial border throughout the cardiac cycle. The clinical feasibility was assessed of the auto EF method for measuring LV volumes and EF in patients. Manually traced EF measured by the biplane modified Simpson's rule was used as the reference standard. METHODS: The study population consisted of 30 consecutive patients with normal sinus rhythm. All patients underwent two-dimensional echocardiography. The auto EF method incorporated pattern and shape recognition to automatically locate the LV, track the endocardium, and calculate EF from routine digital images. LV end-diastolic and end-systolic volumes and EF measured by the auto EF method were compared those by the manually traced method. LVEF by the Auto EF method was also compared with visual EF determined by nonattending physicians. RESULTS: Auto EF was more reproducible than visual EF by the expert reader. LVEF by the auto EF method had excellent correlation and close limits of agreement with manually traced EF compared with visual EF(4-chamber view: y = 1.10 x - 4.28, r = 0.94, bias = 1.6%, 2-chamber view: y = 0.88 x + 7.25, r = 0.90, bias = 0.4%). LV volumes by the auto EF method underestimated those by manually traced EF (end-diastolic volume by 4-chamber view: y = 0.72 x + 8.92, r = 0.93, bias = - 16.7 ml, end-systolic volume by 4-chamber view: y = 0.82 x - 0.97, r = 0.98, bias = - 8.5 ml, end-diastolic volume by 2-chamber view: y = 0.73 x + 12.4, r = 0.82, bias = - 12.3 ml, end-systolic volume by 2-chamber view: y = 0.65 x + 6.94, r = 0.90, bias = - 6.8 ml). CONCLUSIONS: The auto EF method is a clinically useful tool for the measurement of LV volumes and EF.

Left atrial volume: predictor of atrial fibrillation in patients with degenerative mitral regurgitation.

BACKGROUND AND AIM OF THE STUDY: In patients with mitral regurgitation (MR) due to degenerative mitral valve prolapse (MVP), preoperative atrial fibrillation (AF) has been identified as an independent predictor of survival after surgery for MR. Thus, the determinants of preoperative AF may have critical implications to evaluate the timing of mitral valve repair. The study aim was to investigate the role of left atrial (LA) volume in predicting preoperative AF in patients with severe MR due to degenerative MVP. METHODS: Sixty-six patients with severe degenerative MR (regurgitant volume > or =60 ml, regurgitant fraction > or =50%, effective regurgitant orifice area > or =0.4 cm(2)) in sinus rhythm (SR) at diagnosis and conservatively managed were eligible for the study. Complete two-dimensional (2-D) echocardiographic and Doppler measurements, including the measurement of maximum LA volume, were performed in all patients. RESULTS: During follow up under conservative management (18.1+/-4.8 months), eight patients (12%) experienced conversion to AF, and 58 remained in SR. The mean LA dimension was 4.0+/-0.5 cm in patients with SR, and 5.1+/-0.8 cm in those who developed AF (p <0.0001). The mean LA volume and LA volume index (indexed to body surface area) were 95 +/-23 ml and 60+/-14 ml/m(2) respectively in patients with SR, and 166+/-66 ml and 104+/-42 ml/m(2) respectively in those who developed AF (both p <0.0001). The optimal cut-off value for LA volume to predict AF conversion was 117.5 ml (sensitivity 88%, specificity 83%), and for LA volume index was 75 ml/m(2) (sensitivity 88%, specificity 88%). CONCLUSION: LA volume measurement should be considered in patients with degenerative severe MR diagnosed in SR. A LA volume index > or =75 ml/m(2) reflects the risk of subsequent AF, and patients should be closely monitored.

Left atrial volume in normal Japanese adults.

BACKGROUND: Two-dimensional (D) echocardiography-derived left atrial (LA) volume has been shown to provide a more accurate assessment of LA size than the M-mode LA dimension. Our objective was to provide reference ranges of LA volume in healthy Japanese adults. METHODS AND RESULTS: The study subjects consisted of 105 Japanese adults, with a mean age of 39+/-13 years (range 20-63 years old). All subjects had normal ejection fraction (>55%), no wall motion abnormalities, normal diastolic function, no valvular disease, and normal sinus rhythm. The maximum LA volume, at left ventricular end-systole just before the opening of the mitral valve, was measured by using the bi-apical (4- and 2-chamber views) Simpson's rule. Both the absolute LA volume and the volume corrected by body surface area (LA volume index) were obtained. The LA volume ranged from 21 to 53 ml (mean 37+/-8 ml) and the LA volume index ranged from 13 to 30 ml/m(2) (mean 22+/-4 ml/m(2)). The mean LA volume index + 2SDs was 30 ml/m(2). CONCLUSIONS: Recognition of the upper limits of LA volume in normal Japanese subjects is of particular clinical relevance because it offers the opportunity of pathological LA remodeling diagnosis.

Coronary flow velocity pattern assessed noninvasively by transthoracic color Doppler echocardiography serves as a predictor of adverse cardiac events and left ventricular remodeling in patients with acute myocardial infarction.

BACKGROUND: Quantitative assessment of microvascular injury is possible in patients with reperfused anterior myocardial infarction by invasive method. Coronary flow velocity patterns can also be assessed by transthoracic color Doppler echocardiography (TTCDE). OBJECTIVES: The purpose of this study was to determine whether the coronary flow velocity pattern assessed by TTCDE serves as a predictor of adverse cardiac events and left ventricular remodeling. METHODS: The study population consisted of 64 consecutive patients. We could analyze coronary flow velocity patterns by TTCDE in 59 of 64 patients (92%) after coronary intervention. The patients were followed up for the occurrence of complications and underwent serial measurement of left ventricular volumes. RESULTS: In patients with a short deceleration time of diastolic flow velocity, the frequency of adverse cardiac events and left ventricular remodeling was higher. CONCLUSION: It is possible to predict clinical outcome by assessing coronary flow velocity pattern by TTCDE.

Transthoracic Doppler echocardiographic assessment of coronary flow velocity pattern in patient with acute myocardial infarction implies progression of myocardial damage.

BACKGROUND: Coronary flow velocity (CFV) pattern with a rapid deceleration time of diastolic flow velocity and small average systolic peak velocity immediately after reperfusion implies poor wall-motion recovery in patients with acute myocardial infarction. Microvascular injury has been demonstrated to progress after coronary reperfusion. The purpose of this study was to assess whether CFV 1 day after reperfusion (day 1) may reflect accurately the degree of myocardial damage. METHODS: In the left anterior descending coronary artery in 29 patients with anterior acute myocardial infarction, CFV was measured immediately and 1 day after recanalization using transthoracic Doppler echocardiography, respectively. Regional wall motion was estimated as anterior wall-motion score index (AWMSI) by echocardiography before recanalization and 1 month after the onset of acute myocardial infarction. RESULTS: Although significant correlation was observed among deceleration time of diastolic flow velocity, average systolic peak velocity, and average peak velocity immediately after reperfusion and 1-month AWMSI (r = -0.62, P < .001; r = -0.61, P < .001; and r = -0.55, P < .01, respectively), much better correlation was demonstrated between those at day 1 and 1-month AWMSI (r = -0.72, P < .0001; r = -0.68, P < .0001; and r = -0.60, P < .001, respectively). Deceleration time of diastolic flow velocity, average systolic peak velocity, and average peak velocity in poor wall-motion recovery group (1-month AWMSI > 2.0, n = 14) were significantly smaller (P < .01, P < .05, and P < .05, respectively) at day 1 compared with those immediately after reperfusion. CONCLUSIONS: CFV pattern assessed by transthoracic Doppler echocardiography at day 1 provides the degree of myocardial damage much more accurately than that immediately after reperfusion. These results may suggest that myocardial damage progresses after reperfusion.

Annular geometry in patients with chronic ischemic mitral regurgitation: three-dimensional magnetic resonance imaging study.

BACKGROUND: Although animal studies showed that annular remodeling may be related to the pathogenesis of chronic ischemic mitral regurgitation (CIMR), little was known in humans. A better understanding of the precise 3D geometry of the mitral valvular-ventricular complex in CIMR is needed to devise a better surgical technique. The purpose of the study was to elucidate mitral annular geometry in patients with CIMR using cardiac MRI. METHODS AND RESULTS: Thirty-eight patients with previous inferior or posterior myocardial infarction were studied. With the 3D reconstruction of the mitral annulus and subvalvular apparatus from a series of longitudinal cine MRIs, end-systolic mitral annulus dimensions and 3D geometry were calculated. Patients were grouped by mitral regurgitation grade using echocardiography (> or =2+, n=15 versus < or =1+, n=23). Both septal-lateral and commissure-commissure mitral annular diameters were significantly greater in CIMR(+) patients (35+/-5 versus 30+/-4 mm, P=0.005; 46+/-6 versus 39+/-4 mm, P<0.001, respectively). The length of the fibrous annulus was significantly larger in CIMR(+) patients (28+/-3 versus 24+/-3 mm; P<0.001). The height of the annular "saddle horn" above a best-fit plane was lower in CIMR(+) patients (4.2+/-1.2 versus 6.0+/-1.8 mm; P=0.002), and the annular height to commissural width ratio was significantly lower in CIMR(+) patients (12+/-3 versus 21+/-5%; P<0.001). CONCLUSIONS: Patients with CIMR had greater septal-lateral and commissure-commissure mitral annular dimension, larger intertrigonal distance, and flattened saddle shape of mitral annulus. These associated geometric alterations may be important in the pathogenesis of CIMR.