Enhanced levels of oxidized low-density lipoprotein prime monocytes to cytokine overproduction via upregulation of CD14 and toll-like receptor 4 in unstable angina.

OBJECTIVES: The purpose of this study was to establish whether oxidized low-density lipoprotein (oxLDL) contributes to cytokine overproduction via upregulation of CD14 and toll-like receptor-4 (TLR-4) expression on circulating monocytes of unstable angina (UA) patients. METHODS AND RESULTS: Expression of CD14 and TLR-4 on circulating monocytes, and the concentration of plasma oxLDL, (interleukin [IL])-6, IL-1 beta, IL-8, tumor necrosis factor (TNF)-alpha, monocyte chemoattractant protein-1 (MCP-1) were measured in 27 control (C) subjects, 29 patients with stable angina (SA), and 27 with UA. CD14 and TLR-4 expression on monocytes and circulating IL-6, IL-1 beta, and oxLDL were higher in UA than in SA and C subjects (P<0.001). In in vitro experiments, oxLDL increased CD14 and TLR-4 expression (P<0.001) in control monocytes as well as IL-6, IL-1 beta, and at a lower extent TNF-alpha and MCP-1 levels in the supernatant (P from <0.05 to <0.001). The preincubation of sera derived from UA patients but with control monocytes also induced a significant increase of CD14 and TLR-4 expression (P<0.001) and of IL-6 and IL-1 beta production (P<0.001) in the supernatant. CONCLUSIONS: In UA patients oxLDL may contribute to monocyte overproduction of some cytokines by upregulating CD14 and TLR-4 expression.

Left atrial dilatation in systolic heart failure: a marker of poor prognosis, not just a buffer between the left ventricle and pulmonary circulation.

BACKGROUND: The relation between systolic pulmonary pressure (sPAP) and left atrium in patients with heart failure (HF) is unclear. Diastolic dysfunction, expressed as restrictive mitral filling pattern (RMP), and functional mitral regurgitation (FMR) are associated with both LA enlargement and increased sPAP. We aimed to evaluate whether atrial dilation might modulate the consequences of RMP and FMR on the pulmonary circulation of patients with HF with reduced ejection fraction (HFrEF). METHODS: 1256 HFrEF patients were retrospectively recruited in four Italian centers. Left ventricular (LVD) and atrial (LAD) diameters were measure by m-mode, and EF were measured. RMP was defined as E-wave deceleration time lower than 140 ms. FMR was quantitatively measured. sPAP was evaluated based on maximal tricuspid regurgitant velocity and estimated right atrial pressure. RESULTS: Final study population was formed by 1005 patients because of unavailability of sPAP in 252 patients. Mean EF was 33 ± 3, 35% had RMP, 67% had mild, and 26% moderate-to-severe FMR. 69% of patients had increased sPAP. A significant association was observed between sPAP and EF, RMP, FMR, and LAD (p < 0.0001 for all). At multivariate analysis, LAD was positively associated with sPAP (p < 0.0001) independently of EF, RMP, and FMR. Analogously, LAD (p < 0.05) was associated with more severe symptoms and worse prognosis after adjustment for LV function and FMR. CONCLUSION: LA dilation was positively associated with sPAP independently of EF, RMP, and FMR. This highlights that LA size should be considered a marker of the severity of the disease.

The relationship between carotid and coronary atherosclerotic damage in dialysis patients.

BACKGROUND: Data relating carotid ultrasound (CU) to atherosclerotic damage evaluated by coronary angiography in hemodialysis patients are scarce. METHODS: We carried out a cross-sectional study in 33 uremic subjects (age 55 +/- 12 years, 22 male, 7 diabetic), who have been on dialysis for 41 +/- 48 months (range 2-192). Twenty-two underwent a coronary angiography in order to complete clinical evaluation for inclusion on the kidney transplantation waiting list, and 11 because of coronary artery disease (CAD); Gensini's score was calculated. Intima-media thickness (IMT) and presence of plaques were related to the degree of coronary stenosis and to cardiovascular risk factors. Patients were divided into two groups depending on mean IMT (group 1 IM 0.9 mm, n=15). RESULTS: Group 2 was older (60 +/- 8 vs 50 +/- 12 year, p=0.01), had higher frequency of CAD (53 vs 16%, p=0.02) and had higher prevalence of coronary artery stenosis >or= 75% in the right (60 vs 22%, p=0.02), left anterior descending (46 vs 16%, p=0.06) and left circumflex coronary arteriers (60 vs 11%, p=0.05) than group 1. IMT was not related to the degree of CAD evaluated by Gensini's score. IMT sensibility and specificity in detecting the presence of hemodynamically significant coronary stenosis were 64% and 68%, respectively. Coronary narrowing was correlated with the degree of stenosis of common, internal and external carotid arteries (Spearman's rank correlation coefficient). During two years of follow-up, six major cardiac events were recorded and they were related to Gensini's score. CONCLUSIONS: In uremic patients, ultrasonographic evaluation of carotid arteries is a simple, noninvasive examination that could be a helpful tool in detecting coronary atherosclerotic damage, but IMT does not appear to add more information regarding risk stratification of CAD.

Stent implantation versus balloon angioplasty in chronic coronary occlusions: results from the GISSOC trial. Gruppo Italiano di Studio sullo Stent nelle Occlusioni Coronariche.

OBJECTIVES: In this multicenter, randomized trial we evaluated whether stent implantation after successful recanalization of a chronic coronary occlusion reduced the incidence of restenosis. BACKGROUND: Percutaneous transluminal coronary angioplasty (PTCA) in chronic total occlusions is associated with a higher rate of angiographic restenosis and reocclusion than PTCA in subtotal stenoses. Preliminary reports have suggested a decreased restenosis rate after stent implantation in coronary total occlusions. METHODS: We randomly assigned 110 patients with recanalized total occlusion to Palmaz-Schatz stent implantation, followed by 1 month of anticoagulant therapy versus no other treatment. The primary end point was the minimal lumen diameter (MLD) of the treated segment at follow-up, as determined by quantitative angiography at a core laboratory. RESULTS: Repeat coronary angiography was performed 9 months after the procedure in 88% of patients. The MLD (mean +/- SD) at follow-up was 1.74 +/- 0.88 mm in patients assigned to stent implantation and 0.85 +/- .75 mm in patients assigned to PTCA (p < 0.001). Stent implantation was associated with a lower incidence of restenosis (defined as diameter stenosis > or =50% at follow-up) (32% vs. 68%, p < 0.001) and reocclusion (8% vs. 34%, p = 0.003) than balloon PTCA. Likewise, stent-treated patients had less recurrent ischemia (14% vs. 46%, p = 0.002) and target lesion revascularization (5.3% vs. 22%, p = 0.038), but experienced a longer hospital stay. CONCLUSIONS: Palmaz-Schatz stent implantation after successful balloon PTCA of chronic total occlusions improves the midterm angiographic and clinical outcome and could be the preferred treatment option in selected patients with occluded vessels.

Evidence of parasympathetic impairment in some patients with cardiac syndrome X.

OBJECTIVES: Cardiac syndrome X (SX) is a clinical condition characterised by angina, positive exercise stress test and negative coronary angiography; it has often been attributed to sympathetic hyperactivity. Here we tested the hypothesis that a parasympathetic, rather than a sympathetic, dysfunction could be the cause of the autonomic imbalance observed in SX. METHODS: In 20 subjects with diagnosed SX and in 12 age-matched controls, we studied autonomic function by performing spectral analysis of RR interval and finger arterial pressure (SAP), in supine position and during head-up tilting. We also carried out a set of tests of parasympathetic function. RESULTS: The group of SX patients did not differ significantly from control subjects in any of the variables tested. In a subgroup of 13 SX, however, tilting increased the low-frequency power of SAP, but did not induce the expected increase in low-frequency and decrease in high-frequency power of RR. These patients, in supine position, had significantly lower sinus arrhythmia and a higher ratio of low to high frequency of RR, in comparison with control subjects. We interpreted these differences as signs of reduced parasympathetic, but essentially normal sympathetic, activity. The parasympathetic tests confirmed vagal impairment in the same SX subjects. On the other hand, all the tests indicated normal parasympathetic functions in the control subjects and in those SX patients who displayed the expected spectral changes in tilting. CONCLUSIONS: In about two thirds of the patients with SX, the pathophysiological mechanism causing the symptoms could be related to the reduced parasympathetic tone, rather than to an augmented sympathetic activity.

Coronary artery vasomotion and post-stenotic coronary artery blood flow after intracoronary lacidipine in patients with ischaemic heart disease: a pilot study.

BACKGROUND: The calcium antagonist lacidipine has been shown to be highly vasoselective and to improve myocardial perfusion in hypertensive patients. However, its effects on coronary artery vasomotility and on post-stenotic coronary flow reserve in patients with atherosclerotic heart disease are unknown. OBJECTIVES: This study was designed to investigate the acute direct effects of repeated infusions of lacidipine on epicardial coronary artery vasomotion and on post-stenotic coronary artery blood flow in patients with stable angina pectoris and angiographic evidence of coronary heart disease. METHODS: In 8 patients with stable angina and moderate to severe stenosis of the left coronary artery, measurements of epicardial dimensions (quantitative angiography) and of coronary blood flow (Doppler guidewire) distal to a stenosis were performed at baseline and after 3 repeated intracoronary boluses of 12 microg of lacidipine. Results were compared with those obtained after 10 mg of intracoronary papaverine. RESULTS: The intracoronary administration of lacidipine was well tolerated, without any adverse effects. Lacidipine significantly increased the minimal luminal diameter of the lesion (peak relative increase of 43.7%), without significant changes in heart rate and systolic aortic pressure. Intracoronary lacidipine caused a dose-dependent increase in coronary flow reserve. Maximal vasodilatory effects were equivalent to those obtained with intracoronary papaverine. CONCLUSIONS: These results suggest that lacidipine acts directly as a potent vasodilator in stenotic epicardial vessels and improves myocardial perfusion distal to a moderately severe stenosis in patients with stable angina.

Comparison of different pharmacological interventions on enzymatic parameters during acute myocardial infarction.

The concept that acute myocardial infarction is a dynamic event and that different interventions can modify the extent of the necrosis, has led to renewed interest in early pharmacological and surgical treatments designed to reduce the ischemic injury. To evaluate the effects of different pharmacological interventions aimed to reduce the extent of necrosis, we studied 166 patients (138 male and 28 female, mean age of 59.4 +/- 11.3 years) admitted within 6 h after chest pain and treated with a single therapy during the first 72 h. Enzymatic infarct size (IS) was calculated by serial creatine kinase isoenzyme MB determinations using a compartmental model. Six groups of patients were evaluated: 33 patients were treated only with antiplatelet drugs, 38 with anticoagulants, 34 with intravenous thrombolytic therapy, 20 with calcium channel blockers, 25 with nitrates, and 16 with beta-blockers. Estimated IS (gEq/m2) and elimination constant (Kd, U/L/h) did not differ in the six groups, but patients treated with streptokinase had higher release constant (Ka, U/L/h) and shorter time to peak CK-MB value. Early treatment (less than or equal to 2 h after chest pain) had a favourable effect on the enzymatic IS only in patients treated with calcium channel blockers (p less than 0.005).

CPK and CPK-MB in the early diagnosis of acute myocardial infarction and prediction of infarcted area.

This study was carried out on patients of a coronary unit to evaluate the diagnostic efficiency of total CPK and CPK-MB by using different analytical techniques: catalytic, immunoassisted, cellulose acetate electrophoresis, radioimmunoassay and immunoradiometric assay. The behaviour of the enzyme was studied in all patients with reference to the localization and extent of the infarct. In all cases a diagnostic algorithm was followed based on the combined use of CPK and its MB isoenzyme; the activity was measured twice, at three-hour intervals after admission. In this way the utilization of total CPK and MB isoenzyme allows almost complete diagnostic efficiency within the first 9 hours from onset of chest pain, together with the possibility of calculating the slope of the curve of MB isoenzyme release useful for calculating infarct size. Maximum diagnostic efficiency is also obtained in cases of small infarcts, with silent ECG, and those difficult to classify clinically.

Coronary vasoconstriction in response to acetylcholine after balloon angioplasty: possible role of endothelial dysfunction.

BACKGROUND: Abnormal endothelium-dependent vasomotion has frequently been observed early after coronary angioplasty. The aim of this study was to investigate endothelium-mediated coronary vasomotion caused by increasing intracoronary infusions of acetylcholine into epicardial coronary arteries 3-6 months after coronary angioplasty in patients without restenosis (50% luminal diameter reduction). METHODS: Intracoronary acetylcholine was infused during follow-up coronary angiography followed by an intracoronary bolus of 250 g nitroglycerin in 18 patients who had undergone successful angioplasty of 21 isolated coronary artery lesions. Using an automated edge-detection program, coronary artery measurements were performed in the proximal reference segment, in the proximal part of the angioplasty site, at the site of previous maximal stenosis, in the distal part of the angioplasty site, and in the distal reference segment. RESULTS: In the segments of the coronary artery not manipulated by balloon catheter, acetylcholine did not produce significant luminal diameter changes (+2 +/- 23% in the proximal segment and -3 +/- 27% in the distal segment at 10(-4) mol/l). All the angioplasty vessel segments, excluding the proximal reference segments, showed an abnormal dose-related reactivity to the acetylcholine. Maximal vasoconstriction was observed at 10(-4) mol/l and was 4.9 +/- 11.1% in the proximal reference segment, 9.3 +/- 19.1% in the proximal angioplasty site (P = 0.0314), 20.3 +/- 24.1% at the site of previous maximal stenosis (P = 0.0005), 10.7 +/- 16.8% at the distal angioplasty site (P = 0.0098), and 9.3 +/- 14.1% in the distal reference segment (P = 0.0032). The maximal response of the angioplasty site to acetylcholine and to nitroglycerin did not correlate either with the time to follow-up or with the follow-up stenosis. Nitroglycerin-induced vasodilation was significant in all segments, but was lower in the lesion-related segments. Acetylcholine evoked the same effect on both the vessels that were manipulated and those that were not. CONCLUSIONS: Three to 6 months after coronary angioplasty, endothelium-dependent vasodilation was impaired not only at the site of previous maximal stenosis, but also in segments directly injured by balloon inflation. In contrast, endothelium-independent vasodilation by nitroglycerin is maintained in all segments. These observations suggest that the endothelium is still functionally impaired in the area of balloon dilation.

Coronary arterial aneurysms after percutaneous transluminal coronary angioplasty--a not uncommon finding at elective follow-up angiography.

Five coronary arterial aneurysms were found in 4 of 80 (5%) patients who underwent elective coronary arteriography 6 months after successful percutaneous transluminal coronary angioplasty. None of them was present immediately after dilatation. All patients had been suffering from stable angina before angioplasty, while no case had recurrent angina or definite angiographic restenosis at the 6-month follow-up. Quantitative coronary angiography was performed in all angiograms. The coronary aneurysms only developed in the dilated portions (4 in left anterior descending and 1 in an intermediate branch of the left coronary artery): their diameter ranged from 3.1 to 4.4 mm, and their length from 2.2 to 4.9 mm. The ratio between the aneurysm diameter and the coronary arterial diameter (aneurysm: artery ratio) varied from 1.15 to 1.91 (mean 1.47). No significant clinical or technical differences were found between patients who developed aneurysm after angioplasty, and patients who did not. On the other hand, 4 of the 5 patients who developed aneurysm had angiographic evidence of "non-pathologic" dissection immediately after balloon dilatation. Moreover, the ratio between the measured angiographic diameters of the balloon (at maximal inflating pressure) and of the coronary artery selected for the procedure showed that the balloon was mildly oversized (balloon: artery ratio ranging from 1.10 to 1.37, mean 1.28) in all cases with aneurysm except the only 1 in whom dissection did not occur. In conclusion, aneurysm formation after coronary angioplasty is not infrequent in our experience: balloon size and wall dissection seem to be the major factors related to this event.

Effects of the cold pressor test on the left ventricular function of patients with coronary artery disease.

We used the cold pressor test as provocative of myocardial ischemia in 23 subjects evaluated for chest pain on effort. Seven of them (group N) had normal coronary arteries, and 16 (group CAD) had critical stenoses along the main branches of the left coronary artery. In both groups exposure to cold induced increase in arterial pressure and double product. Left ventricular end-diastolic pressure increased +60% from baseline (P less than 0.001). Angiocardiographic parameters, unchanged in group N, showed an impairment of left ventricular function in group CAD. End-diastolic volume increased +11% (P less than 0.01), ejection fraction decreased -8% (P less than 0.0025), with a significant reduction in segmental wall motion in the area of the diseased artery (P less than 0.001). The mean Vcf was slightly and not significantly reduced, while early-systolic and end-diastolic stress and the constant of stiffness consistently increased in both groups. The appearance or extension of ventricular wall contraction abnormalities in group CAD, in the absence of demonstrable coronary spasm and in the presence of a remarkable increase in left ventricular end-diastolic pressure and stress, was interpreted as due to ischemia secondary to increased extravascular resistances to coronary flow. The cold pressor test is proposed as a useful tool for the diagnosis and evaluation of patients with ischemic heart disease.

Update on mechanical revascularization in acute myocardial infarction: which role and when?

Mechanical revascularization in the acute myocardial infarction by primary angioplasty has several advantages over thrombolytic therapy. The short-term patency rates of the infarct-related artery range from 95 to 99% and a normal flow is achieved in more than 90% of the cases. This prompt and effective reperfusion is probably responsible for the improved prognosis with primary angioplasty. The better outcome after primary angioplasty is observed both in low- and in high-risk patients, in all ages and in patients presenting late (>6 h) after the chest pain. Pooled analysis of randomized studies, show that primary angioplasty as compared to thrombolysis, has a lower incidence of death, stroke and reinfarction. Additional advantages of primary PTCA include the possibility of reperfusion in patients in whom lysis is contraindicated or less effective (e.g. patients in cardiogenic shock, or with prior coronary artery bypass surgery) and the ability to provide prognostic information helpful in the patient triage. Thus, primary PTCA results in better outcome than thrombolysis when performed in centers with success rates comparable to those achieved in the randomized trials. Further studies are still needed to assess its long-term efficacy. Several randomized trials are underway to assess the role of stents and the use of more potent antiplatelet drugs, as the GPIIb/IIIa receptor blockers, in adjunct to balloon angioplasty in the treatment of acute myocardial infarction.

The role of activation of the renin-angiotensin system on the reflex regional vasoconstriction caused by distension of the uterus in anaesthetized pigs.

Distension of the uterus in anaesthetized pigs has been shown to cause a reflex regional vasoconstriction and an increase in plasma renin activity (PRA) through efferent sympathetic mechanisms which respectively involved alpha- and beta-adrenergic receptors. The present study was undertaken to determine the possible contribution of the activation of the renin-angiotensin system (RAS) to the observed regional vasoconstrictive responses to uterus distension. In pigs anaesthetized with alpha-chloralose, blood flow in the left circumflex or anterior descending coronary, superior mesenteric, left renal and left external iliac arteries was assessed using electromagnetic flowmeters. Distension of the uterus for periods of 30 min was performed by injecting 20 ml of warm Ringer solution into balloons positioned within the viscus before and after blockade of angiotensin II receptors with losartan. Changes in heart rate and renal blood flows were respectively prevented by atrial pacing and injection of phentolamine into the renal arteries. Changes in baroreceptors activity and in regional perfusion pressure were minimized by section of cervical vagus nerves and denervation of carotid sinuses and by an aortic constriction. PRA was assessed during the last minute of distension by radioimmunoassay of angiotensin 1. Before blockade of angiotensin II receptors, in six pigs, distension of the uterus decreased coronary blood flow by 19%, and in other six pigs, decreased mesenteric and iliac blood flows by 13.1% and 29.4% in the absence of changes in arterial perfusion pressure. After losartan, these decreases were significantly reduced to 11.7%, 8.2% and 18%. These results showed that the activation of the RAS significantly contributed to the alpha-adrenergic receptor-mediated regional vasoconstrictive responses reflexly elicited by distension of the uterus.

Increased mortality after coronary stenting in patients treated with clopidogrel without loading dose. Evidence from a meta-analysis.

AIM: Clopidogrel is an established alternative to ticlopidine in addition to aspirin after coronary stenting because of its hematologic safety, but its efficacy in comparison to ticlopidine is debated. We thus systematically reviewed randomized trials comparing clopidogrel vs ticlopidine after coronary stenting. METHODS: Medline (1/1986-10/2003), BioMed Central, Central, Current Contents, LILACS and mRCT were searched. Fixed-effect relative risks (RR [95% CI]) were computed, and the primary end-point was death. Heterogeneity tests and subgroup analyses were performed according to loading vs non-loading clopidogrel scheme. RESULTS: Five trials were retrieved (2 962 patients, average follow-up 7.4 months). In 3 studies both clopidogrel and ticlopidine were started with a loading dose, in 1 trial clopidogrel was administered without loading, and in 1 trial clopidogrel could be administered with or without loading. Overall analysis (p for heterogeneity=0.12) showed a non-significant trend toward increased mortality in patients treated with clopidogrel (38/1 649 [2.3%]) vs ticlopidine (22/1 313 [1.7%], RR=1.64 [0.94-2.86], p=0.080). After stratification, clopidogrel with loading was associated with non-significantly lower mortality rates than ticlopidine (9/959 [0.9%] vs 13/798 [1.6%], RR=0.68 [0.29-1.63], p=0.39). Instead, clopidogrel without any loading yielded a highly significantly 3-fold increased risk of death than ticlopidine (29/690 [4.2%] vs 9/515 [1.7%], RR=2.9 [1.45-6.1], p=0.0029). Similar results were obtained for the rate of death or non-fatal myocardial infarction. CONCLUSION: This meta-analysis suggests that clopidogrel treatment including a loading regimen is equivalent or may even be superior to ticlopidine after coronary stenting. However, current evidence shows conversely that clopidogrel therapy in the absence of a loading dose is associated with a significantly higher risk of death or myocardial infarction.

[The clinical use of the GPIIb/IIIa inhibitors eptifibatide and tirofiban in the treatment of acute coronary syndromes of the "non-ST elevation" type]. / Impiego clinico degli inibitori GP IIb/IIIa eptifibatide e tirofiban nel trattamento delle sindromi coronariche acute di tipo "non sopraslivellamento del tratto ST".

Acute coronary syndromes not associated with ST-segment elevation, i.e. unstable angina and non-Q wave myocardial infarction, represent a heterogeneous group of clinical disorders sharing similar pathogenic mechanisms, clinical presentation and medical management. Current guidelines recommended an early anti-thrombotic and anti-ischemic treatment in these patients, as well as their prompt risk evaluation based on easily available clinical and instrumental data, to identify those subjects at greater risk in whom a more aggressive management is warranted. Despite the association of aspirin, heparin and anti-ischemic drugs, the 30-day rate of death or myocardial infarction remains high (9-15%) in patients with markers of greater risk (i.e. Braunwald class III, ST-segment depression, abnormal creatine kinase or troponin values). Moreover, in patients with acute coronary syndromes undergoing percutaneous coronary interventions (PCI), complex coronary lesions increase the peri-procedural risk of thrombotic complications. Regardless of the agonist responsible for platelet activation and aggregation, platelet glycoprotein (GP) IIb/IIIa receptor activation is the key factor in thrombosis formation. Several clinical trials in the past few years have documented the beneficial value of GP IIb/IIIa inhibitors in patients treated with aspirin and heparin, with a significant reduction in the cumulative end-point of death and/or myocardial infarction at 48-96 hours (odds ratio--OR 0.81, 95% confidence interval--CI 0.71-0.92, p < 0.01). Such therapeutical benefit is still present at 30 days (OR 0.88, 95% CI 0.81-0.97, p < 0.001) and 6 months (OR 0.88, 95% CI 0.79-0.97, p < 0.001). In patients treated with abciximab, eptifibatide or tirofiban, undergoing early PCI, a remarkable relative reduction in the risk of death and non-fatal acute myocardial infarction was shown before PCI (-34%, p < 0.001). The pre-PCI administration of GP IIb/IIIa inhibitors is associated with a significant reduction in peri-procedural complications (-41% relative reduction of death or acute myocardial infarction in the 48 hours after PCI, p < 0.001). In this subset of patients the benefit correlates with abnormal pre-PCI values of troponin, a reliable surrogate marker of active thrombosis. The greatest clinical benefit from GP IIb/IIIa inhibitors is expected in patients presenting high-risk features (early post-infarction angina; older age with a history of left ventricular dysfunction or diabetes; heart failure symptoms, ST-segment depression, abnormal troponin, creatine kinase, and C-reactive protein values at admission) as well as in patients with recurrent ischemic attacks and those undergoing early PCI. Although the combination of GP IIb/IIIa inhibition and standard doses of unfractionated heparin is associated with an increased risk of major bleeding, such risk can be remarkably reduced adopting simple technical suggestions.

[Myocardial revascularization may resolve arrhythmic warm-up in patients with implantable cardioverter-defibrillator: 2 case reports]. / La rivascolarizzazione miocardica come risoluzione del riscaldamento aritmico in pazienti con cardiovertitotre-defibrillatore impiantabile: due casi clinici]

Patients with ventricular arrhythmias and coronary artery disease may have a poor clinical outcome because of an increased risk of sudden cardiac death. In these patients therapeutic approaches include two main strategies: automatic implantable cardioverter-defibrillator (ICD) and antiarrhythmic drugs (when left ventricular function is preserved). Patients with arrhythmic warm-up sustained by ischemic attacks may be stabilized after percutaneous or surgical revascularization. We report the cases of 2 ICD patients, in whom the correction of myocardial ischemia was successful in preventing further ICD discharges. In the first patient with known coronary artery disease (previous acute myocardial infarction and left ventricular ejection fraction 30%) a sudden arrhythmic warm-up was reported with 70 ICD discharges in 24 hours; the patient underwent coronary artery bypass surgery and only few isolated episodes of ventricular tachycardia were observed during the following 34 months. In the second patient with a history of dorsal acute myocardial infarction and two previous interventions of coronary artery bypass graft surgery, we observed a sudden and unexpected arrhythmic instabilization with several ICD discharges. After percutaneous transluminal angioplasty of a graft stenosis, the clinical situation was stabilized and no more ICD activations were observed during the follow-up. In selected patients arrhythmic warm-up can rely on an ischemic substrate, then a careful re-evaluation for ischemia is mandatory in order to resolve the situation.