永久性心脏起搏对纤溶系统的影响

目的探讨不同模式永久性心脏起搏对纤溶系统的影响。方法随机选择安装永久性心脏起搏器患者54例,根据起搏模式分为两组,其中VVI起搏器36例(V组),DDD起搏器18例(D组)。选择32例起搏器术前患者作对照组(C组)。测定组织型纤溶酶原激活剂(t-PA)活性、a2-纤溶酶抑制剂(a2-PI)活性、纤溶酶原灭活剂(PAI)活性及D-二聚体(D-D)浓度。结果V组和D组的PAI活性明显高于C组(P<0.01),V组和D组之间差异也有统计学意义(P<0.05)。V组和D组的t-PA活性却明显低于C组(P<0.01),其中V组又低于D组(P<0.05)。PAI/t-PA比值的改变与PAI活性改变相似;PAI/t-PA比值与术后时间之间没有线性相关关系(P>0.05)。V组的a2-PI活性高于C组(P<0.05)。各组之间D-D浓度差异无统计学意义(P>0.05)。结论置入永久性心脏起搏器患者纤溶功能处于低下状态,尤其以单腔心室起搏为明显。     

Pacemaker related endocarditis: analysis of seven cases

Vegetative electrode infection following permanent pacemaker implantation is a rare and serious complication. Among 1920 patients who underwent permanent pacemaker implantation in our institute between 1980 and 2000, 7 patients aged 65 to 78 years were diagnosed to have pacemaker related endocarditis. In this study, the clinical course and management strategies for these patients are reviewed. The most frequently encountered factors contributing to development of pacemaker infection were local complications such as postoperative hematoma and inflammation, and recurrent surgical interventions on the pacemaker system. In blood cultures S. aureus was the most common causative microorganism. Echocardiography could be performed in 5 patients. Three patients were referred to open-heart surgery for total removal of the pacemaker system, and one patient had his pacemaker system removed percutaneously. The remaining 3 patients did not agree to either surgical or percutaneous removal. These patients have been under antibiotic therapy for approximately 3 years and they still do not have any signs of a serious infection. Consequently, in patients with permanent pacemakers, infective endocarditis should be considered in the presence of fever and local symptoms. Blood cultures should be obtained and echocardiography should be performed. Complete removal of the pacemaker system with intensive antibiotic treatment is necessary for complete eradication of the infection. However, if percutaneous or surgical removal of the electrodes cannot be done because of high perioperative risk or the patient does not agree to undergo either method, medical treatment with long term antibiotic use may be considered as an alternative.     

Swab cultures accurately identify bacterial pathogens in diabetic foot wounds not involving bone.

AIMS: Current clinical practice assumes swab cultures from wounds are unreliable. However, this assumption is based upon data culled only from wounds in which osteomyelitis and/or gangrene were present. This study aimed to re-evaluate the accuracy of swab cultures vs. deep tissue cultures in diabetic wounds of varying depth and severity. METHODS: A total of 60 infected diabetic foot wounds were cultured. Two specimens were taken from each wound: superficial swab before debridement and deep tissue specimen towards the end of surgical debridement. RESULTS: In 37 wounds (62%), the micro-organisms isolated from the swab specimen and those isolated from the deep tissue specimen were identical. In another 12 wounds (20%), the swab culture contained all micro-organisms isolated from the deep tissue culture, but also contained additional micro-organisms. Analysis according to the depth of the wound, demonstrated that swabs identified all micro-organisms isolated from the deep tissue specimens in 36/40 wounds (90%) that did not extend to bone as opposed to 13/20 wounds (65%) that extended to bone. CONCLUSIONS: Swab cultures are valuable in identifying pathogens in diabetic foot wounds when bone is not involved. When surgical debridement is contraindicated or delayed, swab cultures can be used to select appropriate antibiotic therapy.     

起搏器心内膜炎的外科治疗

目的　介绍 15例起搏器心内膜炎外科治疗的临床经验 ,讨论手术指征和时机。方法　1993年至 2 0 0 1年间 ,我们为 15例起搏器心内膜炎患者 ,施行了体外循环直视下心内起搏电极撤除术。本文对这些病人的临床资料进行回顾性研究。结果　本组病例中 ,有 2例院内死亡 ,术后随访期内 (中间值 =31 3个月 ;区间 ,1 8～ 5 8 7个月 )无远期死亡 ,总死亡率为 13 3%。所有出院病人均无感染复发。大部分病人心功能明显改善 (P <0 0 1)。只有 6例患者术后因持续存在的心律失常需要重新安装起搏器。本组病例中常见的外科手术指征为 :1)附着于起搏电极的大型赘生物 ,2 )顽固感染 ,3)三尖瓣架构损坏 ,4)肺栓塞 ,5 )存在需要外科处理的基础的或并存的心脏病变。结论　根据我们的结果及相关文献报道 ,我们认为对患起搏器心内膜炎的病人 ,应尽早采用外科手术撤除植入的心内起搏器硬件。手术治疗的远期效果是值得信赖的。     

Surgical treatment of pacemaker and defibrillator lead endocarditis: the impact of electrode lead extraction on outcome

BACKGROUND: Cardiac device (CD) endocarditis is an infrequent but potentially lethal infectious complication of permanent pacemakers or implantable cardioverter-defibrillators (ICDs), and mortality rates of 30 to 35% have been reported. Medical treatment has been suggested for the treatment of CD endocarditis, but there is increasing evidence that surgical treatment is to be preferred as the best approach to achieve eradication of the infection and reduce mortality. OBJECTIVE: To evaluate the following: (1) the clinical and echocardiographic characteristics of patients with pacemaker or ICD endocarditis, (2) the outcome of this population depending on the mode of treatment (medical vs surgical treatment), and (3) the clinical, microbiological, echocardiographic, and therapeutic variables associated with patient outcome. DESIGN: Prospective cohort study. SETTING: Tertiary referral center in Barcelona, Spain. PATIENTS: All consecutive patients with infectious endocarditis (IE) admitted to the study institution between 1990 and 2001 were prospectively evaluated by a multidisciplinary treatment team, and a definite diagnosis of CD endocarditis was established when cases met pathologic or clinical criteria according to the Duke criteria. RESULTS: A total of 31 patients, 25 men and 6 women aged 61 +/- 15 years (mean +/- SD), with pacemaker or ICD endocarditis were identified among 669 consecutive patients (4.6%) with IE. During the study period, a total of 3,768 pacemakers and 460 ICDs were implanted in the study institution. In 22 cases of pacemaker endocarditis, the pacemaker was implanted in our institution, and 9 cases were referred from other institutions (incidences of endocarditis on pacemaker and ICD implanted in our institution of 0.58% and 0.65%, respectively). Medical treatment without removal of the pacing system was initially performed on seven patients; all of them (100%) had relapses of endocarditis, and one patient died. The remaining 24 patients underwent surgical removal of the pacing system; 1 patient had one relapse, 3 patients died after surgical treatment, and the others were successfully cured with no relapses after a mean follow-up of 38 +/- 9 months. Clinical, echocardiographic, microbiological, and therapeutic variables were evaluated in association with prognosis. The only prognostic factor for failure of treatment or mortality was the absence of surgical treatment (p < 0.0001). CONCLUSIONS: Electrode lead endocarditis occurred in < 1% of pacemaker and ICD implants. Conservative treatment without explantation of all hardware failed in all patients, and surgical treatment during antibiotic therapy was effective in eradication of infection but was associated with a 12.5% mortality. The only patient characteristic associated with treatment failure or death was the absence of surgical removal of all infected hardware. Complete extraction of the pacemaker or ICD should be considered as standard therapy for most patients with CD endocarditis.     

Pacemaker infection caused by Staphylococcus schleiferi

Pacemaker infection is one of the severe complication of pacemaker implantation. We report a case of pacemaker infection caused by Staphylococcus schleiferi which is a coagulase-negative staphylococcus, and its relation with human infection is not well characterized. In 1994, a 80-year-old male presented with a pacemaker pocket infection, cutaneous inflammation but no fever 2 months after insertion of a pacemaker. S. schleiferi was isolated from the pus. The patient was given cefazolin for 5 days. One month later he was readmitted because of cutaneous inflammation and the extruded generator was removed. S. schleiferi was isolated from the generator. After the patient was treated with cefazolin for 3 weeks, four consecutive wound cultures were all negative. A new generator was inserted on the same side. One month after re-insertion, the patient again presented a cutaneous inflammation, and S. schleiferi was isolated from the pus as well as the generator and the leads on their removal. Twenty-six days later, a new pacing system was inserted on the other side. There was no further recurrence of the infection. Removal of the entire pacing system was necessary to cure the infection. We expect further information of human infections caused by S. schleiferi.     

Pacemaker endocarditis during 18 years in Göteborg

Pacemaker endocarditis is a rare but serious complication. Few studies addressing its treatment have been published. Clinical characteristics and outcome were retrospectively studied in 38 patients with 44 episodes of pacemaker infective endocarditis (PMIE) in G?teborg, during 1984-2001. The male/female ratio of episodes was 27/17 and the mean age 69 y. Transthoracic echocardiography (TTE) showed vegetation in 4/22 (18%) episodes and transoesophageal echocardiography (TEE) in 22/33 (67%). Staphylococci were isolated in 66% of blood cultures. The pacemaker system (PS) was removed in 28 episodes and in 18 of these there were no signs of reinfection at follow-up. In 16 episodes the PS was not removed, and in 13 of these, signs of infection were found at follow-up. Thus, the present study of PMIE showed staphylococci to be predominant causative agents and demonstrated a high diagnostic sensitivity of TEE. According to our results, PM removal rather than conservative treatment should be considered in all cases.     

Infective endocarditis following incomplete ablation of a pacemaker

Pacemaker lead-related infective endocarditis is uncommon but mortality remains high. We report the case of a 63-year-old man who presented with a history of intermittent low-grade fever and no other sign for 15 months. Fever had developed after incomplete removal of a pacemaker with the ventricular lead left in situ followed by a new implantation of cardiac stimulation material. Positive blood cultures and transesophageal echocardiography showing a vegetation on a pacemaker lead gave the diagnosis. Initial antibiotic therapy was insufficient and complete surgical extraction of the pacemaker and leads was required. A huge vegetation was seen on the old ventricular lead. The other leads were not affected. Outcome was good. The paucity of symptoms in pacemaker lead-related infective endocarditis makes diagnosis difficult. It must however be suspected in pacemaker patients with low-grade intermittent fever. Transesophageal echocardiography is required. Treatment must combine antibiotic therapy with material extraction.     

Hierarchy of ventricular pacemakers.

To characterize the pattern of pacemaker dominance in the ventricular specialized conduction system (VSCS), escape ventricular pacemakers were localized and quantified in vivo and in virto, in normal hearts and in hearts 24 hours after myocardial infarction. Excape pacemaker foci were localized in vivo during vagally induced atrial arrest by means of electrograms recorded from the His bundle and proximal bundle branches and standard electrocardiographic limb leads. The VSCS was isolated using a modified Elizari preparation or preparations of each bundle branch. Peacemakers were located by extra- and intracellular recordings. Escape pacemaker foci in vivo were always in the proximal conduction system, usually the left bundle branch. The rate was 43+/-11 (mean+/-SD) beats/min. After beta-adrenergic blockade, the mean rate fell to 31+/-10 beats/min, but there were no shifts in pacemaker location. In the infarcted hearts, pacemakers were located in the peripheral left bundle branch. The mean rate was 146+/-20 beats/min. In isolated normal preparations, the dominant pacemakers usually were in the His bundle, firing at a mean rate of 43+/-10 beats/min. The rates of pacemakers diminished with distal progression. In infarcted hearts, the pacemakers invariably were in the infarct zone. The mean firing rates were not influenced by beta-adrenergic blockade. The results indicate that the dominant pacemakers are normally in the very proximal VSCS, but after myocardial infarction pacemaker dominance is shifted into the infarct. Distribution of pacemaker dominance is independent of sympathetic influence.     

Plasminogen activator inhibitor type 1 deficiency

Summary. Plasminogen activator inhibitor type 1 (PAI‐1) is an important component of the coagulation system that down‐regulates fibrinolysis in the circulation. Reduced PAI‐1 levels may result in increased fibrinolysis and an associated bleeding diathesis. Clear documentation of PAI‐1 deficiency as a cause of a bleeding disorder has been rare. PAI‐1 was initially identified in the 1980s, and the first reported case of PAI‐1 deficiency appeared in 1989. Several reports followed, although only two identified an underlying genetic defect. These reports of PAI‐1 deficiency suggest that affected individuals exhibit mild to moderate bleeding symptoms, including epistaxis, menorrhagia, and delayed bleeding after trauma or surgical procedures. Affected individuals rarely exhibit spontaneous bleeding events commonly seen in other procoagulant deficiencies. The majority of bleeding events are controlled with antifibrinolytic agents, such as tranexamic acid and ε‐aminocaproic acid. A major issue that contributes to difficulty in establishing an accurate diagnosis of PAI‐1 deficiency is that the activity assay is accurate in detection of elevated levels but not at the lowest range. Reported normal ranges begin at zero, thereby making a deficiency state because of a dysproteinaemia difficult to distinguish from that of a normal unaffected individual. Although the antigen assay may be helpful in some circumstances, it assists only with complete quantitative disorders. Because of lack of standardized commercially available PAI‐1 activity assay sensitive in the lowest range, the true prevalence of this rare condition has not been established.     

Candida tropicalis pacemaker endocarditis

A rare case of Candida tropicalis pacemaker endocarditis was diagnosed in a 77-year-old male who presented with lethargy. The organism was isolated from cultures of blood and vegetations on the tricuspid valve, interatrial septum and the pacing wire removed at surgery. The postoperative course was stormy and he succumbed to multiorgan failure.     

Differential regulation of plasminogen activator and plasminogen activator inhibitor by osteotropic factors in primary cultures of mature osteoblasts and osteoblast precursors

Plasminogen activators (PA) and plasminogen activator inhibitors (PAI) have been implicated in the process of extracellular matrix degradation. To study their role in bone matrix turnover, we examined the activity and regulation of PA and PAI in cultures of periosteal osteoblast-like precursor cells and mature osteoblast-like cells from fetal rat calvariae. Both cell populations released PA activity of the tissue type and a 50K PAI species into the culture medium. However, mature osteoblasts had a strikingly lower PA activity and higher PAI activity than periosteal precursor cells, indicating that osteoblast differentiation is associated with a marked decrease in the PA/PAI ratio. PTH and prostaglandin E2 transiently increased PA activity and decreased PAI activity. In contrast, transforming growth factor-beta decreased PA activity and increased PAI activity. Differential effects of these factors on PA and PAI activity may be involved in the regulation of extracellular matrix deposition by osteoblasts.     

A case of Mycobacterium goodii infection wifh isolation from blood and a pacemaker lead

We report a case of blood stream infection due to Mycobacterium goodii in a patient who had an implanting pacemaker. The patient injured left thorax where the pacemaker was implanted several days before septicemia. The microorganism was isolated from both blood cultures and leads of the pacemaker. The serial isolates were identified as M. goodii by conventional biochemical methods, tobramycin susceptibility test and 16Sr-RNA sequencing. This is the first reported case of M. goodii septicemia in Japan. M. goodii is regarded as an environmental bacterium and its pathogenicity has been recognized recently. The present case suggests that its ability as a primary invader should not be underestimated, especially in a patient with indwelling devices.     

上海地区幽门螺杆菌菌株cag致病岛基因cagA、cagE、cagT检出率及临床意义

目的 检测上海地区幽门螺杆菌（Ｈｐ）分离株ｃａｇ致病岛（ＰＡＩ）中ｃａｇＡ、ｃａｇＥ、ｃａｇＴ基因,初步探讨ｃａｇＰＡＩ的完整性及其与胃十二指肠疾病的关系。方法 用多聚酶链反应（ＰＣＲ）技术扩增和检测了９９株从１７例慢性浅表性胃炎、２１例慢性性胃炎、１９例胃溃疡、２３例十二指肠溃疡和１９例胃癌中分离的Ｈｐ菌株的ｃａｇＡ、ｃａｇＥ、ｃａｇＴ基因。结果 ｃａｇＡ、ｃａｇＥ和ｃａｇＴ的总检出率分别为８４．８％（８４／９９）、９９．０％（９８／９９）和８４．８％（８４／９９）,各基因检出率在各种胃十二指肠疾病患者分离的Ｈｐ菌株之间差异无显著性（均Ｐ〉０．０５）。９８株ｃａｇＥ阳性的菌株中,有１４株ｃａｇＡ阴性。结论 上海地区分离ｐ菌株绝大多数可能具有完整的ｃａｇＰＡＩ,其完整性与其感染后的临床结局不相关。ｃａｇＥ基因可     

Fibrinolysis in pregnancy: a study of plasminogen activator inhibitors

During pregnancy the plasma concentration of two different inhibitors of plasminogen activators (PAIs) increases. The only one found in the plasma of nonpregnant women (PAI1) is immunologically related to a PAI of endothelial cells; its plasma activity, as deduced from the inhibition of single-chain tissue-type plasminogen activator (t-PA), increased from 3.4 +/- 2.3 U/mL (mean +/- 95% confidence limits) in the plasma of nonpregnant women to 29 +/- 7 U/mL at term, and its antigen level, measured by a radioimmunoassay, increased from 54 +/- 17 ng/mL to 144 +/- 25 ng/mL. In pregnancy plasma a second PAI (PAI 2) related to a PAI found in placenta extracts was observed. Its level, quantified with a radioimmunoassay, increased from below the detection limit (approximately 10 ng/mL) in normal plasma to 260 ng/mL at term. One hour after delivery, PAI 1 activities and antigen decreased sharply, but the PAI 2 antigen levels remained constant. Three days later, the PAI 1 antigen levels had fallen to normal levels, but the PAI 2 antigen levels were still at least eightfold above the nonpregnant values. During pregnancy, the t-PA and prourokinase (u-PA) antigen concentrations increased 50% and 200%, respectively, whereas the plasminogen and alpha 2-antiplasmin levels remained constant. Despite the large variations in the levels of PAs and PAIs, the overall fibrinolytic activity as measured in diluted plasma by a radioiodinated fibrin plate assay did not change significantly. Just after delivery, a great increase in the t-PA antigen levels was observed. Three to five days after delivery most parameters of the fibrinolytic system were normal again. Our results demonstrate that during pregnancy and in the puerperium profound alterations of the fibrinolytic system occur that are characterized by increases in PAs and their inhibitors, but these alterations do not affect the overall fibrinolytic activity.     

Quantitative analysis of intestinal motor patterns: spatiotemporal organization of nonneural pacemaker sites in the rat ileum

BACKGROUND & AIMS: Intestinal contractions are triggered by electric activity of pacemaker cells within the smooth muscle. However, the precise spatial organization of the pacemaker system is unknown. We directly assessed the spatiotemporal organization of pacemakers by video image analysis combined with manometry and electromyography. METHODS: Isolated segments of rat ileum were perfused arterially with oxygenated fluorocarbon solution and luminally with saline. Luminal end pressures, extracellular electric activity, and images of the intestine were recorded simultaneously. Tetrodotoxin, N(G)-nitro-L-arginine methyl ester (L-NAME), L-arginine, and eserine were administered arterially. RESULTS: Myogenic contractions originated in discrete areas (dominant pacemakers) and propagated faster in aboral than in oral direction. Dominant pacemakers were distributed along the intestine at regular intervals. The preparations were mostly driven by 1 pacemaker at the time, but 2 or 3 pacemakers with different frequencies could be active simultaneously. Tetrodotoxin decreased aboral propagation velocity and revealed multiple regularly spaced pacemaker areas. Eserine increased, whereas L-arginine decreased, their frequency. After L-NAME, pacemaker activity increased and isolated pacemakers with higher frequency appeared. CONCLUSIONS: Nonneural pacemakers in rat ileum are functionally organized not as a continuous system but show a segmental arrangement, spatially and temporally modulated by neural activity.     

Chronic bacterial endocarditis on the electrical catheter in a pacemaker wearer: a clinical case report]

This article reports a case of infective endocarditis in a patient with a permanent pacemaker 15 months after the generator had been replaced. The patient had Staphylococcus epidermidis isolated in several blood cultures. No interventional or clinical procedure with any risk of bacteremia was performed, nor was any infective complication of the pocket observed. Thus, the portal of entry of the etiologic agent is unclear. The role of transesophageal echocardiography in detecting pacemaker-induced endocarditis is very important and therapy of choice involves removal of the pacemaker system as soon as possible.     

Pacemaker infections--treatment with total or partial pacemaker system removal

During the years 1977 to 1983, 1,458 pacemakers were implanted or reimplanted in our clinic. Seventy-nine patients were treated during the same period for pacemaker system infections. The time interval between the preceding surgical maneuver and the manifest infection was 11.9 +/- 10.2 months in the catheter fistulas and 12.2 +/- 11.5 months in the pacemaker pocket infections. Forty-one of 79 infections (52%) occurred following the first generator implantation. In 33/43 (76.7%) patients with partial pacemaker system removal, recurrent infection occurred 19.6 +/- 17.2 months later. The infection was treated with similar surgical maneuvers resulting in subsequent infections in 9 patients after 9.8 +/- 7.2 months. In the patients with total pacemaker system removal infection developed in 2/25 (8%). The infection resulted in septicemia in 9 patients. Major surgical intervention was necessary for removal of the infected endocardial electrode in 7 patients. According to our experience there are no grounds for partial removal of the pacemaker system if infection occurs. The primary results may be satisfactory but re-infection will appear in the majority of the patients after a period of several months.     

Plasminogen activator and plasminogen activator inhibitor in human preovulatory follicular fluid

To evaluate the roles of plasminogen activator (PA) and PA inhibitor (PAI) in human ovulation, we obtained follicular fluid and granulosa cells from individual preovulatory follicles of patients undergoing gamete intrafallopian tube transfer. The follicular fluid samples (n = 25) were analyzed for total tissue-type PA antigen, PA enzyme activity by fibrin autography, PAI activity, PAI type 1 (PAI-1) antigen, and PAI-1 mRNA. The follicular fluid of preovulatory follicles contained low levels of total tissue-type PA antigen (less than 1 ng/mL). Fibrin autography experiments indicated little or no detectable PA activity associated with free or unbound PA. The results of the PAI activity assay and PAI-1 antigen determination support the concept of a relative abundance of PAI compared with PA. Hybridization analysis was used to measure the relative amounts of granulosa cell PAI-1 mRNA. The levels of PAI-1 mRNA correlate with follicular fluid PAI concentrations in individual follicles. Taken together, these results support the idea that there is very little free, or active, PA in follicular fluid of human preovulatory follicles, but there is an abundance of PAI. Furthermore, PAI-1 produced by the granulosa cells may represent a major form of PAI in follicular fluid.     

Temporal Changes in a Novel Metric of Physical Activity Tracking (Personal Activity Intelligence) and Mortality: The HUNT Study,Norway

BackgroundPersonal Activity Intelligence (PAI) is a novel activity metric that translates heart rate variations during exercise into a weekly score. Weekly PAI scores assessed at a single point in time were found to associate with lower risk of premature cardiovascular disease (CVD) mortality in the general healthy population. However, to date, the associations between long-term longitudinal changes in weekly PAI scores and mortality have not been explored.PurposeThe aim of the present study was to prospectively examine the association between change in weekly PAI scores estimated 10 years apart, and risk of mortality from CVD and all-causes.MethodsWe performed a prospective cohort study of 11,870 men and 13,010 women without known CVD in Norway. By using data from the Nord-Trøndelag Health Study (HUNT), PAI was estimated twice, ten years apart (HUNT1 1984-86 and HUNT2 1995-97). Mortality was followed-up until December 31, 2015. Adjusted hazard ratios (AHR) and 95% confidence intervals (CI) for death from CVD and all-causes related to temporal changes in PAI were estimated using Cox regression analyses.ResultsDuring a mean (SD) of 18 (4) years of follow-up, there were 4782 deaths, including 1560 deaths caused by CVD. Multi-adjusted analyses demonstrated that participants achieving a score of ≥100 PAI at both time points had 32% lower risk of CVD mortality (AHR 0.68; CI: 0.54–0.86) for CVD mortality and 20% lower risk of all-cause mortality (AHR 0.80; CI: 71–0.91) compared with participants obtaining <100 weekly PAI at both measurements. For participants having <100 PAI in HUNT1 but ≥100 PAI in HUNT2, the AHRs were 0.87 (CI: 0.74–1.03) for CVD mortality, and 0.86 (CI: 0.79–0.95) for all-cause mortality. We also found an inverse linear relationship between change in PAI and risk of CVD mortality among participants with 0 PAI (P < 0.01), and ≤50 PAI (P = 0.04) in HUNT1, indicating that an increase in PAI over time is associated with lower risk of mortality. Excluding the first three years of follow-up did not substantially alter the findings. Increasing PAI score from <100 PAI in HUNT1 to ≥100 PAI in HUNT2 was associated with 6.6 years gained lifespan.ConclusionAmong men and women without known CVD, an increase in PAI score and sustained high PAI score over a 10-year period was associated with lower risk of mortality.