Effects of Irrigation and Rainfall on the Population Dynamics of Rift Valley Fever and Other Arbovirus Mosquito Vectors in the Epidemic-Prone Tana River County, Kenya.

Rift Valley fever (RVF) is a mosquito-borne viral zoonosis that is found in most regions of sub-Saharan Africa, and it affects humans, livestock, and some wild ungulates. Outbreaks are precipitated by an abundance of mosquito vectors associated with heavy persistent rainfall with flooding. We determined the impact of flood-irrigation farming and the effect of environmental parameters on the ecology and densities of primary and secondary vectors of the RVF virus (RVFV) in an RVF-epidemic hotspot in the Tana River Basin, Kenya. Mosquito sampling was conducted in farms and villages (settlements) in an irrigated and a neighboring nonirrigated site (Murukani). Overall, a significantly higher number of mosquitoes were collected in farms in the irrigation scheme compared with villages in the same area (P < 0.001), or farms (P < 0.001), and villages (P = 0.03) in Murukani. In particular, key primary vectors of RVFV, Aedes mcintoshi Marks and Aedes ochraceous Theobald, were more prevalent in the farms compared with villages in the irrigation scheme (P = 0.001) both during the dry and the wet seasons. Similarly, there was a greater abundance of secondary vectors, particularly Culex univittatus Theobald and Culex pipiens (L.) in the irrigation scheme than in the Murukani area. Rainfall and humidity were positively correlated with mosquito densities, particularly the primary vectors. Adult floodwater mosquitoes and Mansonia spp. were collected indoors; immatures of Ae. mcintoshi and secondary vectors were collected in the irrigation drainage canals, whereas those of Ae. ochraceous and Aedes sudanensis Theobald were missing from these water bodies. In conclusion, irrigation in RVF endemic areas provides conducive resting and breeding conditions for vectors of RVFV and other endemic arboviruses.

Hemodynamic performance of stentless versus stented valves: a systematic review and meta-analysis.

BACKGROUND: Several trials have compared stentless with stented valves following aortic valve replacement (AVR). The goal of this review was to systematically locate, critically appraise, and quantitatively combine results to determine if stentless valves improve cardiac hemodynamics. METHODS: We performed an unrestricted search of Pubmed Medline, EMBASE, CINAHL, the Cochrane databases, and EBM reviews. Article reference lists and online abstracts from major North American conferences were also searched. We included randomized trials of adults undergoing AVR that compared stentless and stented valves. Blinded reviewers performed assessment of trials for inclusion and trial quality. Two individuals performed data extraction independently. Kappa statistics were used to assess reviewer agreement. A random effects model was employed for statistical analyses. Assessments were made for postoperative, early, and late outcomes. Heterogeneity was explored with sensitivity analyses. RESULTS: Eight studies were identified for inclusion in the primary analysis, with four others included in sensitivity analyses. Baseline comparisons between groups revealed no differences. Our primary analyses revealed no differences between groups for assessments of LV mass or mean transvalvular gradients. Secondary analyses showed stentless valves to have lower peak gradients. Sensitivity analyses were supportive of our primary results. Heterogeneity was observed in some comparisons and sensitivity analyses failed to completely explain this heterogeneity. CONCLUSIONS: Stentless valves did not display hemodynamic benefit in terms of LV mass regression or postoperative mean gradients, but do appear to display superior hemodynamics in terms of peak gradients. Further well-designed and adequately powered trials are required to fully address this question.

The pylorus: take it or leave it? Systematic review and meta-analysis of pylorus-preserving versus standard whipple pancreaticoduodenectomy for pancreatic or periampullary cancer.

BACKGROUND: Our objective was to determine the relative effects of pylorus-preserving pancreaticoduodenectomy (PPPD) and standard Whipple pancreaticoduodenectomy (SWPD) in patients with pancreatic or periampullary cancer. METHODS: We searched seven bibliographic databases, conference proceedings, and reference lists of articles and textbooks, and we contacted experts in the field of hepatobiliary surgery. We included published and unpublished randomized controlled trials. We evaluated the methodological quality of trials and, in duplicate, extracted data regarding operative, perioperative, and long-term outcomes. We contacted all authors and asked them to provide additional information regarding the trials. We pooled results from the studies by using a random-effects model, evaluated the degree of heterogeneity, and explored potential explanations for heterogeneity. RESULTS: Six trials that included a total of 574 patients met eligibility criteria. In the pooled analysis, PPPD was 72 minutes faster (P < .001, 95% confidence interval [95% CI], 53-92), with 284 mL less blood loss (P < .001, 95% CI, 176-391) and .66 fewer units of blood transfused (P = .002, 95% CI, .25-1.16). Other perioperative and long-term outcomes did not statistically differ, although the confidence intervals include important differences. CONCLUSIONS: Moderate-quality evidence suggests PPPD is a faster procedure with less blood loss compared with SWPD. Large absolute differences in other key outcomes are unlikely; excluding relatively small differences will, however, require larger, methodologically stronger trials.

Increased coronary vasomotor tone in acute myocardial infarction patients with spontaneous coronary recanalization.

To clarify the role of coronary spasm or dynamic coronary obstruction in the development of acute myocardial infarction (AMI) with spontaneous recanalization (SR), symptoms in 296 patients with AMI admitted within 24 h after the onset of chest pain were analyzed just before and after onset, and coronary angiograms were analyzed soon after onset. Patients were divided into 3 groups according to the initial angiographic findings in the infarct-related coronary artery (IRCA): group 1 comprised 172 patients with total occlusion (TIMI O); group 2 comprised 57 patients with subtotal occlusion (TIMI 1,2); and group 3 comprised 67 patients with SR (TIMI 3). The incidence of SR was 20.3% at 0-4 h after onset, 22.2% at 4-6 h, 19.7% at 6-12 h, 24.0% at 12-24 h, and 36.0% at 24 h or later. The incidence of SR did not increase significantly as time elapsed. The incidence of angina at rest and variable-threshold angina before the onset of infarction was only 16.2% in group 1, but was significantly higher in groups 2 (64.3%) and 3 (61.9%). The incidence of intermittent chest pain at onset in group 1 (8.4%) was significantly lower than in groups 2 (54.5%) and 3 (38.8%). Vasodilation of the proximal normal segment adjacent to the stenotic site of the IRCA induced by intracoronary nitroglycerin was significantly higher in groups 2 (11.7 +/- 1.2%) and 3 (20.7 +/- 2.6%) than in group 1 (4.0 +/- 0.6%). These results suggest that coronary spasm or dynamic obstruction may be involved in the pathogenesis of thrombus formation or coronary obstruction causing AMI in many Japanese patients.

[Prevention of left ventricular aneurysm formation and left ventricular remodeling caused by percutaneous transluminal coronary angioplasty performed 24-48 hours after onset of acute myocardial infarction].

The prevention of left ventricular aneurysm formation and left ventricular remodeling by percutaneous transluminal coronary angioplasty (PTCA) performed 24 to 48 hours after onset of acute myocardial infarction was investigated. Left ventriculography and coronary angiography were performed in 25 patients within 24 hours of onset of acute myocardial infarction. The patients were divided into two groups; reperfusion group (n = 17) and successful PTCA group (n = 8). The reperfusion group and the PTCA group included patients whose infarct-related coronary arteries were successfully reperfused to 99%, Thrombolysis in Myocardial Infarction (TIMI) grade II or III, immediately after coronary thrombolysis. However, the reperfusion group did not include the patients with spontaneous reperfusion or reperfusion after PTCA. The PTCA group consisted of patients who underwent successful PTCA performed within 24 to 48 hours after onset of infarction (mean 28.4 +/- 6.0 hours). Non-reperfusion in the acute phase was defined as TIMI grade 0-I. The size of the ventricular aneurysm in the PTCA group was significantly reduced compared with the reperfusion group (PTCA group 4.2 +/- 8.7%, reperfusion group 27.2 +/- 6.6%; p < 0.01). The increase of left ventricular end-diastolic volume (delta LVEDVI) from the acute to chronic phases was calculated to estimate left ventricular remodeling. There was a significant difference between the two groups in delta LVEDVI (PTCA group 4 +/- 19 ml/m2, reperfusion group 19 +/- 17 ml/m2; p < 0.05). PTCA performed within 24 to 48 hours after onset in patients with acute myocardial infarction and infarct-related coronary arteries, resulting in reperfusion to 99% TIMI grade II or III immediately after coronary thrombolysis, prevents left ventricular aneurysm formation and remodeling.

New collateral flow increasing early after coronary occlusion prevented myocardial necrosis in dogs.

Increases in regional myocardial blood flow (Qm) developing soon after myocardial infarction may minimize myocardial necrosis. To test this hypothesis, Qm in the area surrounding an acutely occluded coronary artery was determined successively over 4 weeks in 11 dogs. Non-radioactive colored microspheres were injected into the left atrium 5 s (Qm at this time is referred to as Q1), 3 h (Q2), 12 h (Q3), and 4 weeks (Q4) after occlusion of the coronary artery. After termination of the experiment, the heart was removed, and Qm and three indices of myocardial necrosis i.e., myocardial creatine kinase activity (CK), infarct size determined by triphenyl tetrazolium chloride stain (TTC), and myocardial fibrosis visualized by Azan-Mallory stain, were determined. Each Qm was expressed as a percentage of normal: Qm (% of normal) = [Q/Qc] ischemic area/[Q'/Qc']non-ischemic area x 100, where Qc indicates Qm determined before coronary occlusion. In the ischemic area of the left ventricle, Q1, Q2, Q3, and Q4 were 25 +/- 3%, 30 +/- 3%, 31 +/- 3%, and 42 +/- 3% of normal, respectively, in the inner layer, and 31 +/- 3%, 52 +/- 4%, 52 +/- 4%, and 77 +/- 6% of normal, respectively, in the outer layers. During the 4-week period, the increase of Qm in the outer layer was greater than that in the inner layer. The inner layer showed a small increase of flow from Q3 to Q4 (9 +/- 2%), but in the outer layer there were greater flow increases from Q1 to Q2 (21 +/- 3%) and from Q3 to Q4 (24 +/- 6%).(ABSTRACT TRUNCATED AT 250 WORDS)

Preservation of high regional blood flow at epicardial rim after coronary occlusion in dogs.

A thin myocardial layer adjacent to the epicardium (epicardial rim) often survives after transmural myocardial infarction. Regional myocardial blood flow (Qm) at this rim may be high enough to maintain myocardial viability during coronary occlusion. To test this hypothesis, we measured Qm in 12 anesthetized dogs during left anterior descending coronary artery occlusion using nonradioactive colored microspheres. Myocardium in the region supplied by the occluded artery was sliced into sections approximately 0.5 mm thick from the epicardial surface to the endocardium, and the Qm in each section was determined. During occlusion, the Qm of myocardium within 0.5 mm of the epicardial surface remained at 74.8 +/- 8.8% of the preocclusion level. Maintenance of this high Qm during occlusion was abolished when an epicardial incision approximately 1 mm deep was made around the occluded area. These findings suggest that Qm is maintained at a surprisingly high level at the epicardial rim after coronary occlusion through epicardial arterial communications, which may be sufficient to maintain myocardial viability.

[Mechanism of discrepancy between mean pulmonary capillary wedge pressure and left ventricular end-diastolic pressure].

It is well known that discrepancies between mean pulmonary capillary wedge pressure (man-PCWP) and left ventricular end-diastolic pressure (LVEDP) exist in the pathological heart with sinus rhythm. We discussed the mechanism of these discrepancies in the aspect of increased LV end-diastolic stiffness. Fifty-two patients observed in this study included 23 with old myocardial infarction (OMI), 4 with hypertrophic cardiomyopathy and 9 with hypertensive heart disease (LVH group), 6 with dilated cardiomyopathy (DCM), and 10 normal subjects (N). All 52 patients had sinus rhythm. Those with significant mitral and aortic regurgitation were excluded. End-diastolic LV stiffness was evaluated by the ratio of increases in LV pressure and volume during atrial systole (delta P/delta V), as proved by cardiac catheterization and cine-angiography. Discrepancies between m-PCWP and LVEDP were 5.9 +/- 4.3 mmHg in OMI group, 4.5 +/- 4.6 mmHg in LVH group, 5.8 +/- 4.5 mmHg in DCM, and 1.6 +/- 1.8 mmHg in N group. These discrepancies correlated well with delta P/delta V (r = 0.74). More significant discrepancies were observed in patients with so-called pseudo-normalized left ventricular inflow velocities proved by pulsed Doppler echocardiography, and in patients with marked concentric LV hypertrophy with increased delta P/delta V. In clinical observation, symptoms of heart failure may be determined by m-PCWP rather than LVEDP. We concluded that discrepancies between m-PCWP and LVEDP were caused by the booster pump function of the left atrium against increased LV end-diastolic stiffness. By the use of apexcardiogram and echocardiogram including the pulsed Doppler method, it was possible to predict these discrepancies non-invasively.

[Preload dependence of atrial contribution: correlation with left ventricular endo-diastolic wall stress].

The correlation between left ventricular end-diastolic wall stress (sigma ed) and atrial contribution was investigated using echocardiography including the pulsed Doppler method and cardiac catheterization with cineangiography in 21 patients with coronary artery disease, 4 with hypertensive heart disease, 3 with hypertrophic cardiomyopathy, 3 with dilated cardiomyopathy, 4 with aortic regurgitation, and 10 normal subjects. The ratio of peak velocities (A/R) in the rapid filling phase (R) and atrial contraction phase (A) was used as the index of atrial contribution. Left ventricular end-diastolic stiffness (delta P/delta V) was calculated by the ratio of increases in left ventricular pressure and volume during the atrial contraction phase. The correlations between A/R and sigma ed, mean pulmonary capillary wedge pressure (m-PCWP), and left ventricular end-diastolic pressure (LVEDP) were analyzed in the 35 patients. Correlations between delta P/delta V and sigma ed and A/R were also analyzed. A/R was inversely correlated with sigma ed (r = -0.75), m-PCWP (r = -0.62) and LVEDP (r = -0.59), suggesting that A/R is influenced significantly by preload. A/R was also inversely correlated with delta P/delta V (r = -0.72). delta P/delta V was significantly correlated with sigma ed (r = 0.92), suggesting that sigma ed is a factor for determining left ventricular end-diastolic stiffness. Left ventricular volume can be increased in patients with low sigma ed by atrial contraction, achieving good atrial contribution. Left ventricular volume will be little increased by atrial contraction in patients with elevated sigma ed despite significant increase of left ventricular end-diastolic pressure, resulting in diminished atrial contribution.(ABSTRACT TRUNCATED AT 250 WORDS)

Residual critical coronary stenosis during myocardial reperfusion is deleterious to myocardial salvage in dogs.

Hyperemia, which occurs immediately after coronary reperfusion, injures the myocardium. Mild coronary stenosis may mitigate this hyperemia and thus may augment myocardial salvage. To test this hypothesis, left anterior descending coronary arteries of dogs were occluded for 3 h. Then, reperfusion was permitted without residual stenosis (group A, n = 17) or with 75% stenosis (group B, n = 10). Regional myocardial blood flow (RMBF) was determined using colored microspheres. Dogs were sacrificed 1 week later to measure myocardial creatine kinase activity (CK) and for staining with triphenyl tetrazolium chloride (TTC). The RMBF measured 5 min after reperfusion increased significantly (inner layer, 171 +/- 16; outer layer, 165 +/- 11% of control) in group A. This hyperemia disappeared in group B (inner, 106 +/- 8; outer, 117 +/- 10% of control). However, the myocardial CK was more preserved (group A: inner, 31 +/- 4; outer, 44 +/- 4%; and group B: inner, 21 +/- 6; outer, 29 +/- 5%), and the infarct size was smaller in group A than in group B (group A: inner, 44 +/- 6; outer, 33 +/- 5; and group B: inner, 53 +/- 10; outer, 58 +/- 7% of the area at risk). We concluded that a residual stenosis of 75% at reperfusion abolishes the hyperemia but does not improve myocardial salvage.

ST-segment re-elevation and left ventricular expansion soon after acute anterior myocardial infarction.

The sum of ST-segment elevation (sigma ST on V2-4) was measured to evaluate ST-segment re-elevation during early convalescence in 57 patients with acute myocardial infarction. Following rapid ST-segment elevation resolution during the first 12 h, sigma ST again increased in many patients without signs of reinfarction or pericarditis, reaching a maximum approximately 5 days after onset. The magnitude of this re-elevation (delta sigma ST) was less than 0.3 mV in 30 patients (group A), and 0.3 mV or more in another 27 (group B). Based upon left ventriculography, the global ejection fraction in group B decreased significantly from 51 +/- 10% at the acute phase to 46 +/- 10% at the chronic phase. No such decreases were seen for group A. Regional ejection fraction in the infarcted portion improved significantly from 28 +/- 13% at the acute phase to 35 +/- 14% at the chronic phase in group A, but did not improve in group B. In addition, the non-infarcted portion in group B showed a significantly reduced regional ejection fraction. These results suggest that myocardial expansion of the infarcted portion may contribute to ST-segment re-elevation, an ominous sign of left ventricular dysfunction soon after acute myocardial infarction.

The importance of good endocardial reflow immediately after reperfusion for myocardial salvage in dogs.

We studied the importance of reflow after reperfusion for myocardial salvage. In 19 open-chest dogs, the left anterior descending coronary artery was occluded for 3h and then reperfused. Non-radioactive colored microspheres were injected into the left atrium to measure regional myocardial blood flow (RMBF). Immediately after occlusion, RMBF was reduced to 23 +/- 2% (of control) in the inner layer and 32 +/- 2% in the outer layer. Five minutes after reperfusion, RMBF was increased to 170 +/- 20% and 156 +/- 11% of control in the inner and outer layers, respectively. One week later, RMBF in the inner layer was reduced to 63 +/- 4% but it was not reduced (100 +/- 6%) in the outer layer. There was a roughly positive correlation between the inner/outer flow ratio measured 5 min after reperfusion and myocardial creatine kinase activity. Myocardial necrosis determined by triphenyl tetrazolium chloride stain varied inversely with the inner/outer flow ratio. These results indicate that good reflow in the inner layer 5 min after reperfusion is a favorable indicator for myocardial salvage.

Effects of residual coronary stenosis on myocardial salvage after reperfusion in dogs.

In order to study the effects of residual stenosis on myocardial salvage, we created 99% coronary stenosis with or without contrast washout delay at reperfusion in six groups of dogs. In Group A (n = 8), the artery was occluded for 1h before being fully reperfused. In Group B (n = 9), the artery was occluded for 1h, then subjected to 6h of 99% stenosis without contrast washout delay. In Group C (n = 8), the artery was occluded for 1h, followed by 1 week of 99% stenosis without contrast washout delay. In Group D (n = 10), again the artery was occluded for 1h, then subjected to 6h of 99% stenosis with contrast washout delay. In Group E (n = 8), the artery was occluded for 7h, then fully reperfused for 1 week. Finally, in Group F (n = 8), the occlusion lasted for a full week. All dogs were sacrificed 1 week after occlusion. In Group A, myocardial creatine phosphokinase activity (CK) in the inner layer was 43.8 +/- 12.5% that of non-infarcted myocardium. Myocardial CK in Group B (46.5 +/- 7.4%) was little different but in Group C it dropped to 26.6 +/- 8.4%, suggesting that 99% residual stenosis is not deleterious if it is continued for 6h or less but that it will result in considerable depletion of myocardial CK, it is is sustained for 1 week. In Group D, myocardial CK dropped markedly to 11.3 +/- 3.7%, little different from that for either Group E (13.3 +/- 2.6%) or Group F (9.3 +/- 3.3%).(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical significance of abnormal Q wave disappearance in acute transmural myocardial infarction.

The clinical features of acute myocardial infarction patients in whom abnormal Q wave disappeared were analyzed. Of 201 patients, 40 (20%) (Group A) showed disappearance of Q wave in serial electrocardiograms. Regional ejection fraction of the infarcted portion improved significantly (from 24 +/- 2 to 34 +/- 4%, p less than 0.001) during chronic phase in Group A, but no such improvement was present in Group B patients who showed no change in the Q wave. Global ejection fraction was greater and percent akinetic segment was smaller in Group A than in Group B at chronic phase. Coronary occlusion occurred more often at segment 7 in Group A; in Group B, occlusion occurred more frequently upstream at segment 6, suggesting Group A had a smaller area of risk. Spontaneous recanalization was more often (57%) and complete occlusion was less frequent in Group A. These indicate that Group A is characterized by a smaller area of risk, smaller infarct size, earlier reperfusion, and greater improvement in wall motion. Twenty-eight patients (70%) of Group A lost Q wave within one month and 12 patients (30%), after 3 months or more. Electrical stunning of the myocardium may be a possible mechanism for the early disappearance of Q waves, and anatomical healing for the late disappearance of Q waves.

[Clinical characteristics of precordial ST-segment depression in acute inferior myocardial infarction].

Assessments of the significance of precordial ST segment depression in acute inferior myocardial infarction (AIMI) have yielded conflicting results. Among 92 AIMI patients admitted within 6 hrs after the onset, 65 showed ST depression, and the remaining 27 showed no ST depression. These depressions were present in all of V1-4 (right type; 17), V2-5 (middle type; 10), V3-6 (left type; 13) and V1-6 (broad type; 25). The clinical severity was Forrester subset I in the majority (89%) of patients without ST change, while complications were prevalent in patients with ST depression, especially in the right type (44% were Forrester subset II-IV). Peak CK was 2,150 +/- 399 U/L in patients without ST depression, but it was elevated to 3,172 +/- 811 in patients with ST depression, especially in the right type (4,506 +/- 499). Wall motion evaluated by echocardiography and QRS scores on ECG also revealed greater abnormality in patients with ST change. The initial right coronary angiogram on admission revealed complete occlusion in 76% of these patients with ST depression of whom all of the right type had completely occluded artery. Abnormal motion of the anterior wall, which suggests remote ischemia associated with AIMI was proved neither by left ventriculography nor echocardiography. Hospital mortality in patients with ST depression (9.2%) was as twice as high as that in those without ST depression (4.6%). We concluded that ST depression in patients with acute inferior infarction may not be indicative of remote ischemia but manifests as a mirror image of a large infarction with a complicated clinical course.

Effects of coronary thrombolysis on left ventricular ejection fraction in patients with acute myocardial infarction.

Left ventriculograms were performed on 65 patients with acute myocardial infarction, once upon admission and again 3 months later. In 29 cases urokinase was injected intravenously and/or intracoronarily. The other 17 were treated without urokinase. In 8 out of 29 patients whose infarct-related coronary arteries remained completely occluded following urokinase therapy, the global ejection fraction was reduced from 54 +/- 3% during the acute stage to 46 +/- 5% during the chronic stage (p less than 0.001). However, for the 21 patients whose coronary arteries were successfully recanalized, the 2 values were the same (52 +/- 2%). The highest global ejection fractions were seen in 19 spontaneously recanalized patients (acute: 54 +/- 2%, chronic: 55 +/- 2%). For the 8 unsuccessful patients, the regional ejection fraction for the infarcted portion was reduced from 20 +/- 5% during the acute stage to 18 +/- 6% during the chronic stage. But for the successful patients there was an improvement from 22 +/- 2% during the acute stage to 27 +/- 2% during the chronic stage. Again, the regional ejection fraction was the highest for the spontaneously recanalized group, being 31 +/- 2% and 36 +/- 3% during the acute and chronic stages, respectively. These results indicate that if the coronary artery remains occluded during the acute stage the reduced left ventricular function continues to deteriorate even more during the chronic stage. Successful coronary thrombolysis, however, might salvage the infarcted myocardium as well as preserve the function of the left ventricle.