A Novel Method to Suppress the Effect of Subdiaphragmatic Activity in 99mTc Myocardial Perfusion SPECT and Evaluation of Its Usefulness Using a Myocardial Phantom.

Background: Smoothing in 99mTc myocardial perfusion single-photon emission computed tomography (SPECT) often increases myocardial artifacts due to subdiaphragmatic activity near the heart. To reduce these artifacts, we developed a new process flow, masking on unsmoothed images (MUS), that includes the extraction of the myocardium by masking before smoothing. Methods: This study evaluated the relationships between matrix sizes and distances to the subdiaphragmatic activity using the MUS method compared to conventional methods using a combination of image reconstruction methods (filtered back-projection [FBP] and ordered subset expectation maximization [OSEM]) with or without corrections (attenuation [AC], scatter [SC], and resolution recovery [RR]) using a myocardial phantom. The results were compared for two matrix sizes (pixel sizes) (128×128 [3.3 mm] and 64×64 [6.6 mm]); four subdiaphragmatic activity distances (5, 10, 15, and 20 mm); and three reconstruction methods (FBP without correction; OSEM with RR; and OSEM with AC, SC, and RR). Results: In the conventional method, increasing distance resulted in interference with myocardial perfusion SPECT evaluation however, the artifacts were less apparent when the MUS method was applied. The images converted to 64×64 did not show the same effect as the 128×128 images, even when RR was used. The MUS method was useful for acquisition at 128×128, along with the use of RR in the reconstruction process. Conclusion: MUS mitigated the effects of subdiaphragmatic activity on myocardial perfusion SPECT, particularly combined with 128×128 acquisitions and iterative reconstruction with RR.

Vasopressin V2 receptor antagonist tolvaptan is effective in heart failure patients with reduced left ventricular systolic function and low blood pressure.

Diuresis is a major therapy for the reduction of congestive symptoms in acute decompensated heart failure (ADHF) patients. Carperitide has natriuretic and vasodilatory effects, and tolvaptan produces water excretion without electrolyte excretion. We previously reported the usefulness of tolvaptan compared to carperitide in ADHF patients with fluid volume retention. The purpose of this study was to examine whether the efficacy of tolvaptan was altered in ADHF patients with reduced left ventricular systolic function and in those with hypotension. A total of 109 hospitalized ADHF patients were randomly assigned to either a tolvaptan or a carperitide treatment group. Baseline clinical characteristics were not different between the two groups. We divided these patients based on the left ventricular ejection fraction (EF) by echocardiography, and blood pressure (BP) at the time of admission. Daily urine volume between the tolvaptan and carperitide groups in patients with preserved EF (≥ 50%) was not different, however, in those with reduced EF (< 50%), the urine volume was significantly higher in the tolvaptan group than in the carperitide group (day 2, 3, 4, P < 0.05 for all). Daily urine volume did not differ between these two groups in the high blood pressure group (BP ≥ 140 mmHg), but was significantly higher in the tolvaptan group than in the carperitide group (day 1, P = 0.021; day 3, P = 0.017) in the low blood pressure group (BP < 140 mmHg). The present study reveals that tolvaptan is more effective than carperitide, especially in ADHF patients with reduced left ventricular systolic function and without hypertension.

Long-term effects and prognosis in acute heart failure treated with tolvaptan: the AVCMA trial.

BACKGROUND: Diuresis is a major therapy for the reduction of congestive symptoms in acute decompensated heart failure (ADHF) patients. We previously reported the efficacy and safety of tolvaptan compared to carperitide in hospitalized patients with ADHF. There were some reports of cardio- and renal-protective effects in carperitide; therefore, the purpose of this study was to compare the long-term effects of tolvaptan and carperitide on cardiorenal function and prognosis. METHODS AND RESULTS: One hundred and five ADHF patients treated with either tolvaptan or carperitide were followed after hospital discharge. Levels of plasma B-type natriuretic peptide, serum sodium, potassium, creatinine, and estimated glomerular filtration rate were measured before administration of tolvaptan or carperitide at baseline, the time of discharge, and one year after discharge. These data between tolvaptan and carperitide groups were not different one year after discharge. Kaplan-Meier survival curves demonstrated that the event-free rate regarding all events, cardiac events, all cause deaths, and rehospitalization due to worsening heart failure was not significantly different between tolvaptan and carperitide groups. CONCLUSIONS: We demonstrated that tolvaptan had similar effects on cardiac and renal function and led to a similar prognosis in the long term, compared to carperitide.

Management strategy of isolated spontaneous dissection of the superior mesenteric artery.

OBJECTIVE: Isolated spontaneous dissection of the superior mesenteric artery (SMA) is very rare among of the visceral artery dissection and its treatment is not established. In this paper we present our experiences and consider the treatment of isolated SMA dissection. METHODS: A retrospective review of our cases from 2005 was performed. Clinical symptoms, radiologic findings and results were evaluated. There were 14 cases of visceral artery dissection, in which all cases were with SMA dissection. There were 12 males and 2 females with a mean age of 57 years (range 41-78 years). RESULTS: We categorized SMA dissection into the six types according to the Sakamoto's and Zerbib's classification. One patient with type VI underwent emergent endovascular surgery with stent. One patient with type VI received thrombectomy and intimectomy with open surgery. One patient with type II underwent aneurysmectomy due to enlarged dissected SMA 3 months later from onset. The other eleven patients were managed conservatively. At follow-up, the diameter of SMA did not enlarged and the length of the dissection significantly decreased to 20.7 ± 15.7 mm from 38.0 ± 15.1 mm at onset (p <0.01). After treatment, imaging indicated the following changes in classification: type I, one patient; type II, 4 patients; type IV, 4 patients; complete remodeling, one patient, all without any event during the follow-up period of 5-82 months. CONCLUSION: Most patients with isolated visceral artery dissection occurred in superior mesenteric artery and can be treated conservatively; however, endovascular or surgical procedures including laparotomy are indicated when there is suspicion of severe mesenteric ischemia. Because the dissection configuration will change, long term follow-up is necessary. (English translation of Jpn J Vasc Surg 2013; 22: 695-701).

Acute heart failure volume control multicenter randomized (AVCMA) trial: comparison of tolvaptan and carperitide.

BACKGROUND: [corrected] Acute decompensated heart failure (ADHF) is a common and highly morbid cardiovascular disorder. Diuresis is a major therapy for the reduction of congestive symptoms. However, most diuretics cause hyponatremia, which is a worsening factor of ADHF patients prognosis. The purpose of this study was to examine the efficacy and safety of tolvaptan, which is a selective vasopressin V2 receptor antagonist and produces water excretion without changes in sodium excretion, compared with carperitide. METHODS AND RESULTS: One hundred and nine hospitalized ADHF patients were enrolled and randomly assigned to tolvaptan or carperitide treatment groups. Subjective symptoms and plasma BNP level were similarly improved by treatment in both groups. Urine volume was significantly higher in the tolvaptan group (P < .05), but volume of water intake was also higher in the tolvaptan group (P < .05). Blood pressure was significantly lower in the carperitide group than in the tolvaptan group after treatment (P < .05). Less adverse events such as worsening heart failure and hypotension requiring drug discontinuation were observed in the tolvaptan group (P = .027). The average drug cost of tolvaptan was lower than that of carperitide (P < .001). CONCLUSIONS: Tolvaptan might be a novel promising agent for ADHF in terms of efficacy and safety compared to carperitide.

Start and initial results of the Fukushima Prefecture acute myocardial infarction registration survey.

Acute myocardial infarction (AMI) remains one of the most serious heart diseases and elucidation of its pathogenesis and advances in treatment strategies have been desired. In 2009, to understand the status of AMI in Fukushima Prefecture for improving treatment outcomes, a new AMI registration survey system was conducted throughout the prefecture. A total of 1,556 cases were registered in the initial 2 years from 2009 to 2010. The hospital-based overall incidence of AMI in Fukushima Prefecture was 37.9 people per population of 100,000 per year. Mortality from AMI within 30 days of onset was 10.2%. We report herein the actual situation of AMI onset and treatment in Fukushima Prefecture based on the initial results of the survey.

Acute myocardial infarction in Fukushima area of Japan.

Although acute myocardial infarction (AMI) is the most serious coronary disease, the background of its onset and the mortality are not fully understood, especially in Japan. From June 1999 to May 2005, we mailed an annual questionnaire to eighteen hospitals in which emergency cardiac catheterization and percutaneous coronary intervention (PCI) were available in the Fukushima area of Japan. A total of 1,590 patients were included. The onset time of AMI had two peaks, i.e., from 9:00 AM to 10:00 AM and 9:00 PM to 10:00 PM. As for reperfusion therapy, four groups were analyzed, the non-reperfusion therapy group (Group N, n = 233), thrombolysis alone group (Group T, n = 80), PCI without thrombolysis group (Group P, n = 1106), and PCI with thrombolysis group (Group TP, n = 151). The in-hospital mortality rate was significantly reduced in Group P (8.4%) compared with that in Group N (33.0%, p < 0.01) and Group T (18.8%, p < 0.01). However, the in-hospital mortality in Group P did not differ from that in Group TP (9.9%). The in-hospital mortality was analyzed by the logistic regression analysis among age, arrival time after onset, peak creatine kinase (CK) values, coronary risk factors, reperfusion therapy, PCI, and thrombolysis. There were significant differences in age (P < 0.01), peak CK values (p < 0.01), hypertension (p < 0.05), and diabetes mellitus (p < 0.01). These results suggest that the onset of AMI may be partly related to human biorhythms, and that PCI would be effective in reducing the in-hospital mortality.

Specificity of vascular reactivity and remodeling after repeated endothelial injury in a swine model.

We investigated the difference in vascular responses and remodeling between coronary and iliac arteries after repeated endothelial denudation. Endothelial denudation of the left anterior descending coronary artery (LAD) and the right common iliac artery (RIA) was repeated 4 times twice a month using a Fogarty catheter in 21 pigs. Vascular responses to vasoactive drugs were evaluated as % luminal diameter changes on contrast angiography 2 weeks after the last denudation. Corresponding nondenuded sites, ie, the left circumflex coronary artery (LCX) and the left common iliac artery (LIA), were used as references. Acetylcholine (1 microg/kg) did not constrict the LCX (0 +/- 1%) and the LAD (1 +/- 1%, P < 0.05), whereas it constricted the RIA (20 +/- 6%) but not the LIA (-3 +/- 3%, P < 0.01). Alternatively, serotonin (10 microg/kg) constricted the LAD strikingly (88 +/- 5%, P < 0.01 versus LCX and RIA), as well as the RIA (35 +/- 10%, P < 0.05 versus LIA). Vasodilator responses to substance P and isosorbide dinitrate were not different after injury in both arteries. The intima-to-media ratio and adventitia-to-media ratio of the relevant site in cross section of tissue sample from LAD were greater than those from LCX, and were more prominent than those from RIA. The results show that vascular tone regulation after the endothelial injury and vascular remodeling might be altered in a vessel-specific manner.

Alterations of alpha-adrenergic modulations of coronary microvascular tone in dogs with heart failure.

BACKGROUND: It remains unclear whether coronary microvascular response to alpha-adrenergic activation alters in chronic heart failure (CHF). METHODS AND RESULTS: We investigated the alpha-adrenergic receptor-mediated effects on coronary pressure-flow relationship (CPFR) in a tachycardia-induced canine heart failure model. The dogs studied were male (29 of 31) and the drugs were given intracoronary. The slope of CPFR during long diastole was evaluated as an index of coronary vascular resistance, during alpha1- or alpha2-adrenergic stimulation or inhibition under anesthesia in the baseline and failing state after 3 weeks of rapid ventricular pacing. Resting coronary blood flow and CPFR did not change in the failing state from the baseline state. Neither alpha1 nor alpha2 stimulation changed the slope of CPFR in the baseline state. However, in the failing state, alpha1 stimulation decreased the slope of CPFR by 23 +/- 5% (P < .05), whereas alpha2 stimulation increased it by 73 +/- 10% (P < .05), which was nearly abolished by pretreatment with NG-nitro-L-arginine methyl ester. CONCLUSION: Alpha2-mediated vasodilatory action, presumably via endothelium-derived nitric oxide release, would be enhanced in the coronary microvascular bed, which may antagonize enhanced alpha1-induced vasoconstriction in CHF.

Correlation between cardiac norepinephrine overflow during exercise and cardiac 123I-MIBG uptake in patients with chronic heart failure.

UNLABELLED: Cardiac (123)I-metaiodobenzylguanidine ((123)I-MIBG) uptake is reduced in chronic heart failure, and its reduction is reported to relate to the decrease in exercise capacity. Reduced (123)I-MIBG uptake may predict an inadequately reduced adrenergic drive to the heart during cardiac sympathetic stimulation, including exercise. However, there is little information about the relationship between cardiac (123)I-MIBG uptake at rest and norepinephrine (NE) release during exercise in relation to the exercise capacity in the failing heart. The aim of this study was to examine whether cardiac (123)I-MIBG uptake at rest can predict cardiac sympathetic activity during exercise in patients with chronic heart failure. We determined how cardiac (123)I-MIBG uptake at rest relates to NE overflow from the heart during symptom-limited graded exercise in such patients. METHODS: Twelve patients (mean +/- SD, 52 +/- 12 y) with chronic stable heart failure performed symptom-limited graded exercise tests under catheterizations with a 4-min stage using a supine bicycle ergometer within 2 wk after (123)I-MIBG imaging. NE concentrations in the arterial and coronary sinus blood (NE(A) and NE(CS), respectively) were measured at each exercise stage, and NE overflow was approximated by the difference between NE(CS) and NE(A) (NE(CS-A)). RESULTS: The left ventricular ejection fraction at rest was 47% +/- 16% and peak oxygen uptake was 17.7 +/- 5.1 mL/kg/min. The heart-to-mediastinum uptake ratio of the delayed (123)I-MIBG image (1.00 - 1.72; mean +/- SD, 1.30 +/- 0.19) correlated with NE(CS-A) at peak exercise (r = 0.80, P < 0.01) and peak heart rate (r = 0.73, P < 0.01) but not with peak oxygen uptake. CONCLUSION: Cardiac (123)I-MIBG uptake of the delayed image can predict the degree of the increase in adrenergic drive to the heart during sympathetic stimuli induced by exercise in patients with chronic heart failure.

Decreased contractility of the left ventricle is induced by the neurotransmitter acetylcholine, but not by vagal stimulation in rats.

There is still controversy with respect to how an increase in vagal tone changes left ventricular (LV) contractility. It is possible that a difference in LV vagal innervation density may affect the inotropic effect. To test this, we examined the effects of vagal stimulation and acetylcholine (ACh) infusion on the rat ventricle, in which LV vagal innervation density is sparse and a negative force-frequency relationship is uniquely observed. To evaluate LV contractility, we developed an in situ Langendorff preparation, in which the effects of changes in afterload, preload, and coronary flow during an intervention were minimized. Both vagal stimulation and ACh infusion significantly increased LV systolic pressure (34 +/- 16%: 36 +/- 22%. respectively) and its maximum positive first derivative with slowing of heart rate (51 +/- 17%: 46 +/- 18%). These effects of vagal stimulation were abolished by pretreatment with atropine. During a fixed heart rate, LV systolic pressure was not changed by vagal stimulation, however, it was decreased slightly but significantly (11 +/- 8%) by ACh infusion. In conclusion, LV contractility changes due to ACh release during vagal stimulation were negligibly small, presumably due to a sparse vagal innervation density in rats, and therefore, a bradycardia-dependent indirect positive inotropic effect may be dominant compared to a direct negative inotropic action during vagal stimulation. Thus, the integrated effect of vagal nerve stimulation on LV contractility is different among species, because it is determined by a direct negative inotropic effect, which depends on the vagal innervation density in the left ventricle, as well as by bradycardia-dependent indirect inotropic changes.

Alterations of endothelium-dependent and -independent regulation of coronary blood flow during heart failure.

Conflicting data concerning the changes in basal coronary blood flow and nitric oxide (NO)-releasing capacity in chronic heart failure may be due to different phases or duration of heart failure. To investigate endothelium-dependent and -independent regulation of coronary blood flow in different phases of heart failure, coronary pressure-flow relationships during long diastole were obtained before and after rapid pacing of 3 and 5 wk at 240 beats/min in 12 or 6 dogs. Neither basal coronary blood flow nor the slope of coronary pressure-flow relationships changed; however, zero-flow pressure increased slightly after rapid pacing. Intracoronary injection of N(G)-nitro-L-arginine methyl ester decreased coronary blood flow at a perfusion pressure of 50 mmHg by approximately 20% at baseline, 55% after 3 wk of rapid pacing, and 20% after 5 wk of rapid pacing. Acetylcholine-induced increase in coronary blood flow was maintained for 3 wk but was finally attenuated after 5 wk of rapid pacing. In contrast, the coronary blood flow response to adenosine gradually decreased with time. These results suggest that basal coronary blood flow is maintained until the late stage of heart failure, presumably by an increases in NO production during the early stage and then by other vasodilatory substances during the late stage, and that endothelium-dependent vasodilation via exogenously administered acetylcholine in resistance vessels is not necessarily impaired in the early stage despite the gradual reduction of endothelium-independent vasodilation via adenosine in chronic heart failure.