Search

Aims This study aimed to elucidate the long‐term effect of cibenzoline therapy on cardiovascular complications and prognosis in patients with hypertrophic obstructive cardiomyopathy (HOCM). Methods and results Eighty‐eight patients with HOCM were treated with cibenzoline (Group A), and 41 patients did not receive cibenzoline (Group B). The changes in left ventricular (LV) remodelling, incidences of cardiovascular complications and deaths, were examined. The mean follow‐up period was 15.8 ± 5.6 years in Group A and 17.8 ± 7.2 years in Group B. In Group A, the LV pressure gradient (LVPG) decreased immediately after treatment, and the reduction was maintained throughout the study. In Group B, the LVPG decreased gradually according to the deterioration of LV function. LV reverse remodelling was confirmed in Group A, and LV remodelling advanced in Group B. In Group A, the incidence of each cardiovascular complication was

Aims This study aimed to evaluate the changes in left ventricular remodelling with time in patients with hypertrophic cardiomyopathy (HCM) using thallium‐201 myocardial scintigraphy. Methods and results Forty‐eight patients with HCM participated in the study. The extent score (ES) and a newly devised index termed the ‘mean count change’ (MCC) were used to evaluate the myocardial perfusion defects. Using the amount of thallium‐201 uptake (TU), MCC (%) was calculated using the following formula: (last TU − initial TU)∕initial TU × 100. To confirm the site of the lesion, the left ventricle was divided into five segments: anterior, septal, inferior, lateral, and apex. Cardiovascular complications and deaths were recorded. The mean follow‐up period was 8.6 ± 2.0 years. ES increased from 17.4 ± 13.7% to 44.0 ± 22.3% (P

It is unclear whether afterload mismatch occurs during the initial stage of essential hypertension (EHT). Additionally, critical left ventricular hypertrophy (LVH) between preserved and reduced systolic functions in hypertension is also unclear. Thus, we aimed to clarify these points.Forty-five normal control subjects (NCS) and 140 EHT patients participated. EHT patients were subdivided into three groups: group I, without LVH (n = 37); group II, with LVH (n = 80); and group III, with LVH and LV heart failure (LVHF) (n = 23). Routine electrocardiographic and echocardiographic parameters, V5R/V6R ratio, relative wall thickness (RWT), LV mass (LVM) index, and peak systolic wall stress (PSWS) were measured.In group I, LV systolic functions were preserved despite the increase of PSWS. In group II, LVH advanced, but LV systolic functions remained normal. A negative T-wave was observed in 69% of group II and 100% of group III. A significant correlation between RWT and LVM index was seen in NCS and groups I and II (rAfterload mismatch did not occur in group I, but it was observed in group III due to the exhaustion of preload reserve.

We herein report two cases of potentially life-threatening arrhythmia due to hyperkalemia triggered by the excessive consumption of "Hoshi-Imo" (dried sweet potato). Both patients with chronic renal disease on renin-angiotensin-aldosterone system inhibitors presented at the emergency room with non-specific symptoms. Electrocardiograms revealed potentially life-threatening arrhythmia due to hyperkalemia in both cases: sinus arrest with a ventricular escape rhythm, tall and peaked T waves; and a widened QRS complex in a nearly sine-wave configuration without discernible P wave. Both patients fully recovered after intensive care for hyperkalemia. Physicians should recognize the excessive consumption of "Hoshi-Imo" may lead to the development of life-threatening arrhythmia, especially in patients with risk factors for hyperkalemia.

A 70-year-old Japanese man presented with a massive cardiac tumor associated with diffuse large B-cell lymphoma. Standard chemotherapy resulted in complete remission and the cardiac tumor disappeared. (Level of Difficulty: Intermediate.), Central Illustration

Aim This study investigated the relationship between the initial diuretic response to tolvaptan and clinical predictors for tolvaptan responders in patients with acute decompensated heart failure (ADHF). Methods and results Patients (153) with ADHF (clinical scenario 2 or 3 with signs of fluid retention) who were administered tolvaptan were enrolled. Tolvaptan (15 or 7.5 mg) was administered for at least 7 days to those patients in whom fluid retention was observed even after standard treatment. The maximum urine volume immediately after tolvaptan administration showed good correlations with the ejection fraction and estimated glomerular filtration rate that were independent predictors of the urine volume (UV) responders (≥1500 mL increase in urine volume). The diuretic response (in terms of maximum diuresis) diminished with advancing chronic kidney disease (CKD) stage and concomitant deterioration of the renal function. Furthermore, advanced CKD was a significant negative predictor for the body weight (BW) responders (2.0% decrease in the body weight within 1 week after starting tolvaptan). As compared with non-CKD, the presence of advanced CKD predicts poor diuretic response for both UV and BW responders. Conclusions The diuretic response following tolvaptan administration gradually diminished with progressive deterioration of the CKD stage. Worsening renal function was not observed. Tolvaptan is effective in treating CS2 or CS3 ADHF patients who present fluid retention and congestion, suggesting its potential efficacy for fluid management in the ADHF patients with CKD without worsening the renal function.

Intraprocedural stent thrombosis (IPST) is a rare complication of percutaneous coronary intervention that leads to poor outcomes; however, the factors contributing to IPST remain largely unknown. Accordingly, we used intravascular ultrasound (IVUS) to examine the lesion characteristics in patients with IPST. We retrospectively analyzed 1,504 consecutive stent-implanted lesions in 1,324 patients (326 with ST-segment elevation myocardial infarction [STEMI], 403 patients with non-ST-segment elevation acute coronary syndrome [NSTE-ACS], and 595 patients with stable angina). Of these, IPST occurred in 5 patients during percutaneous coronary intervention (0.4% per patient; 3 with STEMI, 2 with NSTE-ACS). The IVUS characteristics of plaques that developed IPST were compared with those of controls without the evidence of IPST (non-IPST; n = 15) who were matched by age, gender, lesion location, and clinical presentation (STEMI, NSTE-ACS, or stable angina). All 5 lesions that led to IPST had ruptured plaques with positive remodeling and attenuation. Plaque rupture was also observed in 40% of the non-IPST group. Multiple plaque ruptures in the culprit lesion were more common in the IPST group (80% vs 7%; p0.01). The maximum cavity area was larger in the IPST group than in the non-IPST group having plaque rupture (4.6 mm(2) [interquartile range, 4.3 to 6.5] vs 2.4 mm(2) [1.8 to 2.9]; p0.01). In conclusion, we found using IVUS that multiple plaque ruptures with larger cavities more often evolved into IPST.

The influence of shunts between the coronary artery (CA) and the left ventricle (LV), on chest pain (CP) in patients with hypertrophic cardiomyopathy (HCM) is unknown. We examined the incidence of CA–LV shunts and their influence on CP in HCM patients. Twenty normal control subjects (NCS), 3 with CP due to CA–LV shunts (CP patients), and 60 with HCM participated. Interventricular septal wall thickness (IVST), LV posterior wall thickness (LVPWT), cardiac and stroke indexes (CI and SI), LV end-diastolic pressure (LVEDP), and proximal diameters of the CA were measured. Twenty-five HCM patients had a CA–LV shunt (41.7%). Both IVST and LVPWT were greater in the HCM patients than in NCS and CP patients. These values showed no significant differences between the HCM with shunt and HCM without shunt groups. CI and SI were lower in the HCM patients than in NCS and CP patients. LVEDP was higher in the HCM and CP patients than in NCS. CA diameters were larger in the HCM and CP patients than in NCS. CP was found in 32 HCM patients (53%). The incidence of CP was greater in the HCM with shunt group than in HCM without shunt group (80 vs. 34%, p

An impaired myocardial perfusion state after primary angioplasty is a strong predictor of long-term adverse outcomes in patients with STEMI. We assessed the relationship between culprit plaque characteristics and myocardial perfusion state after primary angioplasty in patients with ST-segment elevation myocardial infarction (STEMI).A total of 101 consecutive patients with de novo STEMI were divided into 3 groups according to the state of myocardial perfusion assessed by ST-segment elevation resolution (STR): Group A (complete: STR ≥ 70%, n=26), Group B (partial: STR70% but ≥ 30%, n=55) and Group C (none: STR30%, n=20). We analyzed plaque features by virtual histology intravascular ultrasound (VH-IVUS) and assessed the relationship between culprit plaque characteristics and STR after primary angioplasty.Total plaque volume was significantly higher in Group C than in Groups A and B (146.4 ± 38.0 mm(3)vs. 93.3 ± 29.1 mm(3) and 105.8 ± 31.5 mm(3), p0.001, respectively). Necrotic core (NC) volume was also significantly higher in Group C than in Groups A and B (25.4 ± 8.0m m(3), vs. 11.9 ± 6.3 mm(3) and 17.3 ± 9.7 mm(3), p0.001, respectively). Analysis of receiver-operating characteristic curves revealed that total plaque volume and NC volume had the best diagnostic accuracy of all the VH-IVUS parameters to predict STR30%. The optimal cutoff values (sensitivity/specificity) were 123.4 mm(3) (75.0%/75.3%) for total plaque volume and 20.3mm(3) (75.0%/74.1%) for NC volume.Culprit plaque with large plaque burden and high NC volume is closely associated with poor STR after revascularization.

In recent years, while therapeutic outcome after percutaneous coronary intervention is improving due to the introduction of drug-eluting stent and device development, procedure-related complications including coronary perforation may ineluctably occur though at low-frequency, even if careful manipulations are performed under IVUS guidance. Meanwhile, coronary pseudoaneurysm subsequent to coronary perforation is one of the complications at chronic phase infrequently experienced following percutaneous coronary intervention. To date, the incidence and natural history of pseudoaneurysm following coronary artery perforation remain unclear. We experienced a case with coronary pseudoaneurysm developed 2 weeks after Ellis II-type coronary artery perforation which spontaneously disappeared 4 months later. As the mechanism of disappearance, thrombotic occlusion was confirmed upon intravascular ultrasound.

A 44-year-old man was implanted with a sirolimus-eluting stent in the proximal left anterior descending artery 8 years previously. Six years later, multi-slice computed tomography and angiography confirmed the formation of a coronary artery aneurysm around the stent. Optical coherence tomography revealed organized thrombi within the stent. Eight years after implantation, the patient presented with chest pain, and multiple imaging modalities revealed thrombotic occlusion within the stent. Surprisingly, the coronary artery aneurysm became a detour for distal flow from the occluded stent. Long-term follow-up after implantation of first-generation drug-eluting stents is mandatory, because unexpected reactions can suddenly occur. .

Summary Background The angiographic no-reflow phenomenon after primary percutaneous coronary intervention (PCI) carries a poor prognosis in patients with ST-segment elevation myocardial infarction (STEMI). However, the type of plaque composition that associates with the angiographic no-reflow phenomenon remains unclear. Methods A total of 44 patients with STEMI were enrolled in this study. After thrombectomy with an aspiration catheter, virtual histology intravascular ultrasound (VH-IVUS) of the infarct-related vessel was performed. Patients were divided into two groups according to final thrombolysis in myocardial infarction (TIMI) flow grade at the completion of PCI procedure. Complete reperfusion group (CR-group) was defined as final TIMI flow grade 3, and no-reflow group (NR-group) was defined as final TIMI flow ≦2. The relationship between plaque composition and angiographic no-reflow phenomenon was analyzed. Results The angiographic no-reflow phenomenon was observed in 20 individuals. The summation of the percentage of fibrofatty + necrotic core and fibrofatty + dense calcium was significantly higher in the NR-group. Receiver-operating characteristics analysis revealed that the summation of the volume and percentage of fibrofatty + necrotic core (>20.1 mm 3 , 26.2%) and fibrofatty + dense calcium (>20.0 mm 3 , 22.6%) predict the angiographic no-flow phenomenon. Conclusion The fibrofatty-rich component with necrotic core or dense calcium derived from VH-IVUS is closely related to the angiographic no-reflow phenomenon observed in primary PCI.

Takotsubo cardiomyopathy is a cardiac syndrome characterized by reversible left ventricular wall motion abnormalities. It mimics the acute coronary syndrome; however, significant obstructive coronary artery disease is absent. The prognosis is relatively favorable in many cases, but complications may occur during the acute stage. Herein, we present a case of takotsubo cardiomyopathy in a 76-year-old woman. Three days after admission for persistent chest pains, the patient suddenly developed right hemiplegia, right homonymous hemianopsia, and aphasia. By diffusion-weighted magnetic resonance imaging and magnetic resonance angiography, we diagnosed acute-phase cerebral infarction caused by abrupt occlusion of the left middle cerebral artery by a thrombus, and treated it with intravenously administered tissue plasminogen activator. Three hours afterward, the patient's condition improved considerably. She was discharged 15 days after admission without any neurological sequelae. Thus, we show that takotsubo cardiomyopathy complicated by cerebral emboli can be successfully treated using tissue plasminogen activator.Learning objective: Serious complications sometimes occur during the acute stage of takotsubo cardiomyopathy. Cerebral thromboembolisms are relatively common complications of takotsubo cardiomyopathy that require careful observation during acute phase, and anticoagulant therapy needs to be considered. In case of cerebral emboli, rapid treatment by tissue plasminogen activator infusion may lead to a favorable prognosis..

A 16-year-old boy stayed in Tokyo near Yoyogi Park for extracurricular high school activities. After returning home, he experienced an episode of fever and visited our emergency outpatient unit. He initially exhibited symptoms of leukopenia, thrombocytopenia and concomitant rhabdomyolysis and after admission simultaneously developed a biphasic fever and systemic erythema. Based on the results of reverse transcription polymerase chain reaction testing, he was finally diagnosed with dengue fever. After an absence of 70 years, dengue fever has reemerged as a domestic infection. Awareness of this trend led to our diagnosis.

Background Cibenzoline, a class Ia antiarrhythmic drug, is useful for reducing the left ventricular pressure gradient (LVPG) in patients with hypertrophic obstructive cardiomyopathy (HOCM). However, chronic effects of cibenzoline on LVPG and left ventricular (LV) remodeling are unknown. Methods Forty-one patients with HOCM participated in this study. Echocardiographic, electrocardiographic, and brain natriuretic peptide (BNP) data collected before and after cibenzoline treatment were compared. From the relation between LVPG and plasma concentration of cibenzoline, an efficacious plasma concentration of cibenzoline was estimated. Results The mean follow-up period was 74.2 ± 47.1 months. The LVPG decreased from 104.8 ± 62.6 mmHg to 27.6 ± 30.5 mmHg (p

Background: During the remodeling process after myocardial infarction (MI), the expression of proinflammatory cytokines is enhanced in the myocardium. However, only a few clinical studies have been conducted on cytokine involvement in left ventricular (LV) remodeling after MI. Hypothesis: Circulating proinflammatory cytokines may be involved in LV remodeling in patients with reperfused MI. Methods: We studied 25 patients with acute anterior MI who had undergone coronary reperfusion therapy, and 10 normal control subjects with no cardiac disease. In all patients, LV ejection fraction, end-diastolic volume index (EDVI), and end-systolic volume index (ESVI) were determined using left ventriculography at the acute phase and 6 months after onset. The ΔEDVI and ΔESVI were calculated as the value of LV volume reduction, suggesting LV reverse remodeling. Serum levels of interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha were measured using enzyme-linked immunosorbent assay. Results: Serum levels of IL-6 and TNF-alpha at the acute phase were significantly higher in patients with MI than in control subjects (both p < 0.05). The IL-6 levels correlated well negatively with ΔEDVI (r = 0.779, p = 0.039), whereas no correlation was found for TNF-alpha. According to multivariate analysis, IL-6 at the acute phase was a significant independent predictor for LV remodeling after reperfused MI (p = 0.007). Conclusions: Circulating IL-6 levels correlated closely with LV geometric changes during the remodeling process in patients with reperfused MI. Our study addresses the usefulness of another marker for LV remodeling after MI.

Study objectives: Of the hypertrophic obstructive cardiomyopathies, midventricular obstruction (MVO) often has been overlooked. In this study, hemodynamic parameters in patients with MVO were compared with patients with idiopathic hypertrophic subaortic stenosis (IHSS), following which the specific markers for diagnosis of MVO were examined. Patients and design: Twenty healthy control subjects (mean [ SD] age, 54 8 years), 20 patients with MVO (mean age, 54 13 years), and 12 patients with IHSS (mean age, 58 12 years) participated in this study. Hemodynamic parameters associated with carotid pulse tracing (CPT) and echocardiography were examined. Measurement and results: Left ventricular ejection time (LVET) and left ventricular pressure gradient (LVPG) were greater in patients with IHSS than in patients with MVO (p < 0.0001 for both). However, left ventricular dimensions and interventricular septal thickness did not vary between patients with MVO and those with IHSS. As specific markers for the diagnosis of patients with MVO, two specific CPT patterns, the “spike-and-dip pattern” and the “spike-and-half-dome pattern,” were identified, but no specific markers were observed echocardiographically. Among patients with MVO, both LVPG and LVET were greater in patients with the spike-and-half-dome pattern than in patients with the spike-and-dip pattern (113 34 vs 57 17 mm Hg, respectively [p < 0.0001]; 318 19 vs 281 27 ms, respectively [p 0.0033]), but echocardiographic parameters revealed no significant differences between the two types of MVOs. The pattern of continuous-wave Doppler recordings of the left ventricle in patients with the spike-and-halfdome pattern was identical to that of patients with IHSS, but that of patients with the spike-and-dip pattern exhibited concavity from the onset of systole to the point of maximal velocity. Conclusions: Two specific patterns for the diagnosis of patients with MVO were identified by CPT. These patterns may be strongly related to differences in ejection dynamics. (CHEST 2003; 124:1275–1283)

A case of severe aortic stenosis with normal coronary arteriograms was associated with myocardial infarction involving the circumferential subendocardial wall of the left ventricle. The infarct was caused solely by the severe aortic stenosis and resulted from the extreme disparity between myocardial oxygen supply and demand.

Study objectives We sought to assess the incidence of transient U-wave inversion during vasospasm of the left anterior descending coronary artery (LAD) with ST-segment depression as opposed to that with ST-segment elevation. Design Retrospective study. Setting Cardiology division of acute-care hospitals. Patients We studied 49 patients with vasospastic angina whose vasospasm was induced in the LAD, not in the left circumflex coronary artery, by intracoronary injection of acetylcholine. Measurements and results The ECG traces obtained during acetylcholine-induced vasospasm of the LAD were examined. Based on the direction of ST-segment shift, the patients were categorized into two groups: the ST-segment elevation group (n = 27) and the depression group (n = 22). There were no differences in age, gender, or cardiovascular risk factors between the two groups. The distribution of the spastic site in the LAD was also similar. A total reduction in luminal diameter during a provoked attack was more often observed in the ST-segment elevation group than in the ST-segment depression group (37% vs 9%, p = 0.02). Collateral circulation to the LAD was found in only one patient in each group. There were no differences between the two groups in heart rate, systolic BP, and double product of heart rate and systolic BP during the attack. The incidence of acetylcholine-induced anginal attack with U-wave inversion in the ST-segment depression group was nearly as high as that in the ST-segment elevation group (77% vs 78%, p > 0.99). Conclusions The development of transient U-wave inversion during vasospasm of the LAD induced by intracoronary injection of acetylcholine does not depend on the magnitude of myocardial ischemia as judged by the direction of ST-segment shift.

We describe an elderly case of idiopathic dilatation of the right atrium in which right-sided heart failure was exacerbated by drug-induced bradyarrhythmia. An 84-year-old man, who had a 10-year history of episodic edema, was treated with proscillaridin and verapamil hydrochloride at another hospital. He had experienced a poor appetite and general malaise 2 months previously, and exertional dyspnea 10 days previously. On admission, he had jugular venous dilatation, systemic edema, and hepatomegaly. On auscultation, a third heart sound originating from the right ventricle and systolic murmur of tricuspid regurgitation were heard. An admission electrocardiogram showed an atrial standstill and junctional escape rhythm with a QRS rate of 31 beats/minute. Chest roentgenogram revealed a bilateral pleural effusion and cardiomegaly with a cardiothoracic ratio of 76%, but no pulmonary congestion. Echocardiogram disclosed idiopathic dilatation of the right atrium and secondary tricuspid regurgitation. He was given a diagnosis of right-sided heart failure due to idiopathic dilatation of the right atrium exacerbated by bradyarrhythmia, which was suspected to derive from the side effects of proscillaridin and verapamil hydrochloride. Thus, these agents were withheld. In addition, the patient reduced sodium intake and was treated with diuretics and beta-adrenergic agonist. Thereafter, right-sided heart failure markedly improved. At the time of the last follow-up 16 months after discharge, he felt well.

A physician in practice referred a 52-year-old woman to our hospital for a closer examination of systolic murmur. She reported nothing particular. Auscultation showed ejection-type murmur of Levine 2/VI maximally heard at the fourth left sternal border that seemed to be functional. ECG and chest x-ray film showed no abnormal findings. To confirm the cause of systolic murmur, echocardiography was performed. Routine echocardiography indicated that the sizes and functions of both left and right ventricles and valvular functions were normal, so we diagnosed her systolic murmur as functional. Figure 1 shows apical 2-chamber views of a B-mode echocardiogram. As shown in Figure 1A (Movie I in the …

Establishing a symptom–rhythm correlation in patients with unexplained syncope is complicated because of its sporadic, infrequent, and unpredictable nature. Recently, an implantable loop recorder (ILR) has become available to evaluate undiagnosed recurrent arrhythmic episodes particularly in unexplained syncopes, and its usefulness has been reported in patients with recurrent syncopes that remain unexplained after conventional work-up. A 65-year-old man was referred to our hospital for loss of consciousness with nocturnal paroxysmal seizures. He had experienced several similar episodes. No family history of sudden death was evident, and apparent structural heart disease was absent. Coronary angiography with intracoronary ergonovine provocation showed vasospasm in left coronary artery without organic stenosis. Ventricular tachyarrhythmias were not induced by programmed electrical stimuli. According to the guideline, he was at once categorized as having class IIb indication for implantable cardioverter defibrillator implantation. However, his symptoms were not relieved despite administration of anti-anginal medications including nitrates and calcium antagonist. Implantation of an ILR was performed and revealed an episode of ventricular fibrillation during generalized-convulsion attack during sleep. ILR is useful in determining the presence of fatal arrhythmias during syncope, although conventional diagnostic testing, such as electrocardiogram, Holter monitoring, and external loop recording, is inconclusive.

SummaryBackgroundPlaque rupture plays a critical role for the development of acute myocardial infarction. However, whether quantitative parameters with regard to the cavity size of ruptured plaque are associated with no-reflow (NR) phenomenon following primary angioplasty remains to be elucidated.Methods and resultsA total of 53 patients with de novo ST-elevation myocardial infarction (STEMI) who had plaque rupture at the culprit lesion defined by pre-intervention virtual histology intravascular ultrasound (VH-IVUS) were enrolled. Patients were divided into two groups according to the presence of NR phenomenon: NR group (n=19) and non-NR group (n=34). By VH-IVUS, we evaluated cavity length, maximum area, and volume of ruptured plaque in culprit lesions. The cavity length, maximum area, and volume were significantly higher in the NR group than those of the non-NR group (4.8±2.1mm vs. 2.9±4.8mm, p

A 78-year-old man who suffered from syncope and light-headedness during straining. The patient visited to our department for evaluation of his symptom. Cardiac auscultation revealed a grade II/IV systolic murmur along the left parasternal border. Electrocardiography showed T wave inversion at the right precordial leads. Echocardiography demonstrated an unruptured aneurysm originating at the sinus of Valsalva protruding into the right ventricular outflow tract. Cardiac cathtererization demonstrated a pressure gradient of 34 mmHg between the right ventricular cavity and pulmonary artery with a large aneurysm originating from the right coronary cusp. Because of his low activity of daily living owing to old cerebral infarction, we managed the patient conservatively.

A case of severe aortic stenosis with normal coronary arteriograms was associated with myocardial infarction involving the circumferential subendocardial wall of the left ventricle. The infarct was caused solely by the severe aortic stenosis and resulted from the extreme disparity between myocardial oxygen supply and demand.

Of the hypertrophic obstructive cardiomyopathies, midventricular obstruction (MVO) often has been overlooked. In this study, hemodynamic parameters in patients with MVO were compared with patients with idiopathic hypertrophic subaortic stenosis (IHSS), following which the specific markers for diagnosis of MVO were examined.Twenty healthy control subjects (mean [+/- SD] age, 54 +/- 8 years), 20 patients with MVO (mean age, 54 +/- 13 years), and 12 patients with IHSS (mean age, 58 +/- 12 years) participated in this study. Hemodynamic parameters associated with carotid pulse tracing (CPT) and echocardiography were examined.Left ventricular ejection time (LVET) and left ventricular pressure gradient (LVPG) were greater in patients with IHSS than in patients with MVO (p0.0001 for both). However, left ventricular dimensions and interventricular septal thickness did not vary between patients with MVO and those with IHSS. As specific markers for the diagnosis of patients with MVO, two specific CPT patterns, the "spike-and-dip pattern" and the "spike-and-half-dome pattern," were identified, but no specific markers were observed echocardiographically. Among patients with MVO, both LVPG and LVET were greater in patients with the spike-and-half-dome pattern than in patients with the spike-and-dip pattern (113 +/- 34 vs 57 +/- 17 mm Hg, respectively [p0.0001]; 318 +/- 19 vs 281 +/- 27 ms, respectively [p = 0.0033]), but echocardiographic parameters revealed no significant differences between the two types of MVOs. The pattern of continuous-wave Doppler recordings of the left ventricle in patients with the spike-and-half-dome pattern was identical to that of patients with IHSS, but that of patients with the spike-and-dip pattern exhibited concavity from the onset of systole to the point of maximal velocity.Two specific patterns for the diagnosis of patients with MVO were identified by CPT. These patterns may be strongly related to differences in ejection dynamics.

Study objectives: This study assessed whether the antiplatelet agent cilostazol, which has potent cyclic nucleotide phosphodiesterase type-3 inhibitory activity, affects the ventricular escape rate and neurohumoral factors in patients with third-degree atrioventricular block. Design: Prospective, but nonrandomized, study. Setting: Cardiology division of an acute care hospital. Patients: We studied 12 patients with third-degree intra-His or infra-His atrioventricular block who were in functional class II or III of the New York Heart Association classification. None of the patients had experienced Adams-Stokes attacks. Interventions: These patients were given cilostazol orally at a dose of 200 mg daily for at least 1 week. Measurements and results: Before and after treatment with cilostazol, continuous 24-h ECG monitoring and measurement of plasma natriuretic peptide concentrations were performed. Cilostazol significantly increased the mean (± SEM) total 24-h QRS count from 57,300 ± 2,800 to 74,400 ± 3,200 beats (p = 0.001) and significantly decreased the maximum geometric mean R-R interval over a 24-h period from 1,900 ms (95% confidence interval [CI], 1,700 to 2,100 ms) to 1,600 ms (95% CI, 1,400 to 1,900 ms; p = 0.02), although none of the patients showed the abolishment of the atrioventricular conduction abnormalities. The total 24-h count of premature ventricular beats was not different before treatment (15 beats; 95% CI, 5 to 44 beats) and after treatment (12 beats; 95% CI, 5 to 30 beats; p = 0.57). Treatment with cilostazol significantly decreased the concentration of plasma atrial natriuretic peptide from 88 pg/mL (95% CI, 49 to 160 pg/mL) to 51 pg/mL (95% CI, 32 to 80 pg/mL; p = 0.007) and of brain natriuretic peptide from 166 pg/mL (95% CI, 71 to 389 pg/mL) to 77 pg/mL (95% CI, 30 to 178 pg/mL; p = 0.02). Conclusions: Cilostazol significantly increased the ventricular escape rate and significantly decreased the level of circulating natriuretic peptides. Thus, cilostazol could be safely given to selected patients over the short term with third-degree atrioventricular block.