Prevalence and outcome of bacterial endocarditis in patients with implantable cardiac devices infections

Cardiac device infection [CDI] is a devastating complication of permanent pacemakers [PPM] or implantable cardioverter-defibrillators [lCD]. The incidence and outcome of endocarditis among patients [Pts] with CDI is not well defined. Is to report the experience in the prevalence, clinical presentations and management of bacterial endocarditis [BE] among patients with CDI in a tertiary care cardiac center over 25 years. A total of 2630 cardiac devices implanted in a cohort of 2367 patients [pts] over 25 years were studied. Out of these, 117 [4.4%] Pts presented with CDI. Clinical, bacteriologic and both transthoracic [TTE] and transoesophageal Echocardiographic [TEE] assessments were done. Of the 117 Pts with CDI [90 males, age ranging 18-82 yrs, mean=63 +/- 6 ys], 87 [74%] had redo procedures [battery replacement in 50, repositioning of leads in 12, device extrusion in 15 or evacuation of significant haematoma in 10 pts]. Of these 87 pts, 65 had re-implants on the same day of explantation. In 30 pts [26%] no apparent cause of P1 was identified. Out of the 117 Pts with CDI, 30 pts [26% of CDI and 1.1% of total procedures] had device-related BE with vegetations appeared in all pts by TEE [15 DDD, 9 VVI, 3 CRT and 3 lCD]. The clinical presentations were prolonged fever in 25 pts [83%], significant pulmonary hypertension with thrombo-embolism in 3 pts [10%], severe sepsis and multi-organ failure in 2 pts [6%]. Twenty-eight pts [93%] had positive blood cultures Istaph.aureus in 23 [77%] and enterococci in 5]. There were only 2 Pt with negative blood cultures. Device lead vegetations were evident in 20 pts [>10mm diameter in 13 pts]. Ten pts presented with only right heart valves vegetations. Out of the 30 BE pts, 28 [93%] had P1 while 2 pts had no apparent cause but frequent intravenous injections [one drug addict and one on regular haemodialysis]. Out of the 20 pts with lead endocarditis 15 had their leads removed surgically with re-implantation of either epicardial [6 pts] or endocardial leads [9 pts]. Fifteen pts had only medical treatment with proper antibiotics [5 pts with lead BE and all 10 pts with valvular BE]. Four pts [13%] died; all had their devices implanted on same day of explanation. Conclusion: Cardiac devices Redo procedures are major risk factors for CDI specially re-implantation on same day. Device related BE carries a serious morbidity and mortality yet surgical removal of the whole system is the management of choice. Blood stream bactraemia is a potential risk factor in patients with cardiac devices and warrant prophylaxis against BE

Facilitated percutaneous coronary interventrion: a new treatment strategy for acute myocardial infarction

Restoring patency of infarct related artery [IRA] is the ultimate goal which can be achieved either pharmacologically [using thrombolytic therapy] or mechanically [through percutaneous coronary intervention [PCI]. The latter needs a sophisticated setup, an equipped Cath. Lab. and a skilled team. Such a system might not be always available, and a full dose thrombolytic therapy is the next best alternative. Recently there is a trend towards "facilitated PCI" whereby low dose thrombolytic and/or antiplatelet therapies are used prior to primary PCI, aiming at an early, complete, and sustained epicardial flow and myocardial perfusion. To compare the efficacy and safety of facilitated PCI with standard primary PCI, we studied 40 pts with acute myocardial infarction [AMI] divided into 2 groups. A study group consisted of 20 pts [18M, 2F, mean age 46.3 +/- 11.5y], all received 750.000 u of streptokinase combined with GP IIb/IIIa receptor inhibitor "tirofiban" 0.4ug/kg/min over 30min followed by 0.1ug/kg/min over 48 hours. Twenty pts [15M, 5F, mean age 54 +/- 8.6y] served as control group [no thrombolytic nor antiplatelet therapy]. Both groups underwent PCI within [73 +/- 18min] from randomization. Angiographic patency was expressed in terms of TIMI flow grading system, ECG criteria comprised extent and rapidity of ST segment resolution and laboratory criteria involved early peaking of CK-MB within 12 hours from randomization. Besides clinical evaluation in terms of major adverse cardiac events [MACE], echocardiographic parameters [LVEDD and LVEF] were used to assess LV function before and after PCI and monthly thereafter for 6 months. Compared to the group subjected to PCI alone, those who had preceding adjunctive pharmacological therapy "facilitated PCI" exhibited significantly greater TIMI 3 flow [84%: vs 60%, p<0.05], smaller LVEDD [5.0 vs 5.5, p<0.05], significantly higher LVEF [55.4% vs 50.7%, p<0.05] and lower rate of MACE [0% vs 20%]. Patients with facilitated PCI also exhibited significantly higher ST segment resolution, [58% vs 45%, p<0.05] and earlier peaking of CK-MB [85% vs 35%] compared to control group. Facilitated PCI offers an excellent way of circumventing the time delay preceding PCI that is frequently encountered on hospital admission of pts with acute MI. Through combining interventional, fibrinolytic and GP IIb/IIIa inhibitor therapy, facilitated PCI provides a more rapid, complete and sustained patency of IRA than primary PCI alone without the adverse effects of full dose thrombolylic therapy and a with better outcome in terms of lesser MACE and preserved LV function

RVoutflow tract pacing versus RV Apical pathophysiologic Effects and prognostic implications

Right ventricular apical pacing has been reported to be associated with adverse haemodynamic effects and alternative sites of pacing have been recommended. On the other hand RV septal pacing was claimed to be more physiological. The present work is intended to compare the classic right ventricular apical DDD pacing to RV outflow tract [RVOT] pacing in both normal and diseased hearts. We studied 30 patients [pts] with complete heart block [CHB]. Fourteen pts [Group I] had no underlying heart disease [8M and 6F with mean age 64.1 +/- 6.4, range 54-76 years] and 16 [Group II] had heart disease [10M, 6F, with mean age 67.5 +/- 8.9, range 58-86 years] including DCM in 12, 1HD in 3 and RHD in Ipt. Right ventricular apical pacing was conducted in 7pts from group I and 8pts from group II. RVA was conducted in 7pts of group I and 8pts of group II. Besides clinical evaluation, all pts were subjected to 2D echo before, and 6 months after pacing. Echo parameters studied included LVEDD, LVESD, EF% and CO with effects expressed in terms of% changes in various parameters. Compared to RVA pacing RVOT pacing in group I [pts with normal heart] induced insignificant% decrease in LVEDD [2.4 +/- 4.8vs 8.6 +/- 9.3, p value =0.146] or LVESD [4.6 +/- 7.8vs 8.3 +/- 6.0,p value =0.113] and insignificant increase in EF [2.4 +/- 4.6vs 0.42.6, p value =0.113] and CO [2.8 +/- 8.0vs 3.3 +/- 3.5, p value =0.08]. However in RVOT pacing in group II [pts with disease heart] induced significantly greater% decrease in LVEDD [3.0 +/- 2.8vs 1.2 +/- 2.3, p=0.005] in LVESD [3.7 +/- 0.9vs 2.5 +/- 2.3, p=0.000], and significantly greater% increase in EF [8.9 +/- 3.3vs I.7 +/- 1.2,p=0.001] and CO [5.8 +/- 9.6vs 10.7 +/- 18.3, p=0.04] in comparison to RVA pacing in group II In the presence of underlying cardiac dysfunction, DDD pacing by RVOT lead is hemodynamically more advantageous to classic RV apical pacing in terms of improving dimensions and enhancing systolic function. We recommend RVOT pacing in the presence of underlying HD to avoid the so called pacing-induced cardiomyopathy.

Primary versus delayed PCI after acute MI: effect on ventricular remodeling and function

It has been well established that early restoration of patency of IRA by percutaneous coronary intervention [PCI] with recent myocardial infarction [MI] may preserve left ventricular [LV] global function and also prevent LV remodeling. There were controversies however concerning the possible benefits of delayed [within 30 days] restoration of patency of infarct-related artery of patients. To evaluate and compare the results of primary versus delayed PCI in patients with acute MI. Forty patients [35 males, 5 females mean age 50.9] were included in the study with first anterior MI, and were divided into 2 groups. Group A[20 pst] who had the chance of undergoing primary PCI within a mean 5.4 hrs from the onset of chest pain with a door to balloon time 1.6 hrs and group B[20pts] with delayed hospitization [i.e>12 hours] who nether received thrombolytic nor primary PCI, but were scheduled for routine PCI with a mean of 20.7 days. The LV function and dimensions were assessed by serial echocardiographic readings measuring LV end diastolic volume [LVEDV], LV end systolic volume [LVESV], ejection fraction [EF], regional wall motion scoring index [RWMI] at 24hrs of admission and after 3 and six months. At 3 months compared to delayed PCI group, group showed significant improvement in RWMI [from 1.9 +/- 0.3 to 1.27 +/- 0.13 in group A vs 1.6 +/- 0.2 to 1.38 0.18 in group B, p value 0.032]. There was a non significant increase in LVEDV values in the two groups, [from 101 +/- 17.6 to 109 +/- 20.1 in group A vs 98.3 +/- 22.3 to 106.3 +/- 22.1 in group B, p 0.062]. The change in EF values was nearly the same in both groups; [59.6% +/- 3.9 at base line to 58.5% +/- .5 in group A vs 57.1%9.3 to 55.2% +/- 6.4 in group B]. At six month, there was no more improvement in the RWMI in both groups but the group B showed marked increase in LVEDV [from 98.3 +/- 22.3 at base line to 138 +/- 32.96, i.e. 28.9% increase versus 15% increase in the group A [from 101 +/- 17.6 at base line to 115 +/- 32.14, p=0.041]. Where the EF% value was nearly preserved in group A [59.6% +/- 3.9 at base line to 59.9% +/- 6.81], there was remarkable deterioration in the EF% in the delayed group [from 57.1 +/- 9.3 at base line to 51.8 +/- 10.8, p 0.008] after six month. Despite the enthusiasm to the concept of restoring patency of infarct related artery irrespective of time, our data showed that early and immediate revascularization [primary PCI] is superior to delayed intervention. Therefore prompt restoration of patency is highly recommended for myocardial salvage and preserving LV function

Cardiac involvement in primary antiphospholipid syndrome and anticardiolipin positive systemic lupus erythematosus

Since the recognition of antiphospholipid syndrome [APS], many cardiac manifestations have been reported in association with the anti-phospholipid [aPL] antibodies. The APS syndrome can be either primary or secondary to an underlying condition, most commonly systemic lupus erythematosus [SLE]. Echocardiographic studies have disclosed heart valve abnormalities in about a third of patients with APS. The aPL antibodies have been suggested to be a pathogenetic factor in the cardiac abnormalities. To evaluate prospectively the prevalence of cardiac abnormalities in patients with SLE and primary antiphospholipid syndrome [PAPS], and correlate these data with serum level of anticardiolipin [aCL] antibodies. Sixty three patients with SLE [62 females and 1 male] were enrolled and divided into two groups according to the presence [Group III, n=35] or absence of aCL [Group II, n=28]. Ten patients with PAPS [7 females and 3 males] were recruited [Group IV, n=10]. In addition, 23 healthy age and sex matched controls, were included [Group I] The serum levels of IgG and IgM aCL antibodies were measured for all patients and controls by a st and ardized ELISA test. All patients and controls also, underwent st and ard two-dimensional and Doppler echocardiographic examination within a week of serum testing. The aCL IgG antibodies were positive in 30 of 63 [47.6%] patients with SLE, in all 10 [100%] patients with PAPS, and in 1 of 23 [4.5%] control individuals. The aCL IgM antibodies were positive in 12 of 63 [19%] patients with SLE, in 4 of 10 [40%] patients with PAPS, and in none of the control individuals. Both IgG and IgM aCL antibodies were positive in 7 of 63 [11%] patients with SLE and in 4 of 10 [40%] patients with PAPS. Echocardiographic findings showed normal heart in all control subjects [group I], and in 16 [57%] of SLE patients with absence of elevated aCL levels [group II], 10 [28.5%] of SLE patients with elevated aCL levels [group III] and 3 [30%] of patients with PAPS [group IV]. Valvular lesions were detected in 7 patients [25%] in group II, 15 [43%] in group III and 7 [70%] in group IV. Pericardial effusion was SLE: systemic lupus erythematosus, PAPS:primary antiphospholipid syndrome, aPL:anti-phospholipid antibodies, aCL:anticardiolipin antibodies. detected in 3 patients [11%] in group II, 10 [28.5%] in group III, and 1 [10%] in group IV. Myocardial dysfunction was detected in 1 patient [3.5%] in group II, 7 [20%] in group III and 2 [20%] in group IV Left ventricular hypertrophy was detected in 2 patients [7%] in group II, 5 [14%] in group III and 1 [10%] in group IV. Pulmonary hypertension was detected in none [0%] of patients in group II, 4 [11.5%] in group III and 2 [20%] in group IV Diastolic dysfunction was detected in 12 patients [43%] in group II, 14 [40%] in group III and 4 [40%] in group IV. Valvular lesions, myocardial dysfunction and pulmonary hypertension in patients with PAPS and SLE are associated with elevated aCL antibodies. There was no significant difference in the frequency of cardiac involvement between patients with increased aCL antibodies in SLE and those with PAPS. Thus, aCL may play an important role in the pathogenesis of valvular lesions as well as myocardial abnormalities