Injecting a ventricular tachycardia into the heart-Α unique case report.

INTRODUCTION: A 52-year-old woman presented with a complex ventricular arrhythmia in an intraoperative context, during kyphoplasty for an osteoporotic fracture of a lumbar vertebra. The subject showed no indications of a previous cardiovascular condition. METHODS AND RESULTS: Causes of arrhythmias associated with the procedure were excluded. Due to her positive family history for dilated cardiomyopathy, upcoming thoughts were made for unmasking a previous asymptomatic cardiomyopathy. Nevertheless, an intracardiac cement embolism was diagnosed and, finally, the patient underwent an open-heart surgery with successful removal of the cardiac cement. Νo new arrhythmia recorded during follow up. CONCLUSION: To the best of our knowledge, this is the first reported case of ventricular arrhythmogenic presentation of a cardiac cement embolus after a KP procedure.

The long non-coding RNAs MHRT, FENDRR and CARMEN, their expression levels in peripheral blood mononuclear cells in patients with essential hypertension and their relation to heart hypertrophy.

Long non-coding RNAs (lncRNAs) participate in the modulation of cardiac hypertrophy, and they represent potential therapeutic targets in cardiovascular disease. We investigated the expression profiles of selected lncRNAs in peripheral blood mononuclear cells of patients with essential hypertension in relation to left ventricular hypertrophy. We assessed the expression levels of the lncRNAs MHRT, FENDRR and CARMEN using real-time reverse transcription polymerase chain reaction. Hypertensive patients showed significantly higher MHRT, FENDRR and CARMEN expression levels compared with healthy controls. In addition, we observed significant negative correlations of MHRT (r = -0.323, P = 0.003) and FENDRR (r = -0.380, P = 0.001) and a positive correlation of CARMEN (r = 0.458, P < 0.001) expression levels with left ventricular mass index. Our data reveal that the lncRNAs MHRT, FENDRR and CARMEN show distinct expression profiles in hypertensive patients and they possibly represent candidate therapeutic targets in hypertensive heart disease.

Long-term serial changes in platelet activation indices following sirolimus elution and bare metal stent implantation in patients with stable coronary artery disease.

BACKGROUND: Platelet activation is crucial in the development of stent thrombosis following percutaneous coronary intervention (PCI). We carried out a long-term assessment of multiple factors implicated in the thrombotic process and monitored markers of platelet activation after the implantation of sirolimus-eluting stents (SES) in patients with stable coronary artery disease (CAD). Additionally, we compared these findings with those after bare-metal stent (BMS) implantation. METHODS: A cohort of 47 consecutive patients, aged <70 years, with severe stenosis (>70% narrowing of the lumen) of one major epicardial coronary artery and stable CAD underwent successful elective PCI. Patients were randomly allocated to SES (n = 25) or BMS (n = 22). Venous blood was obtained 24 hours before and 24 hours, 48 hours, 1 month, and 6 months after PCI for measurements of plasma levels of sP-selectin, von Willebrand Factor (vWF), fibrinogen, d-dimer, sCD40, factor VIII, b-thromboglobulin (b-TG) and platelet factor 4 (PF-4). RESULTS: There were no significant differences between the two groups in levels of fibrinogen or d-dimers in peripheral blood. However, we observed a significant kinetic effect (p<0.001) and stent-effect (p<0.015) on vWF levels and a significant kinetic effect (p = 0.012) on factor VIII, sP-selectin (p = 0.04), b-TG (p<0.001), and PF4 (p = 0.016). A trend towards a significant stent effect on sCD40 was also detected (p = 0.06). CONCLUSIONS: SES and BMS did not show significant differences in relationship to markers of platelet activation and coagulation in patients with stable CAD. Although some markers showed an increase after stent implantation, they returned to the initial levels 6 months later.

Hypertrophic and antihypertrophic microRNA levels in peripheral blood mononuclear cells and their relationship to left ventricular hypertrophy in patients with essential hypertension.

MicroRNAs regulate several aspects of physiological and pathologic cardiac hypertrophy, and they represent promising therapeutic targets in cardiovascular disease. We assessed the expression levels of the microRNAs miR-1, miR-133a, miR-26b, miR-208b, miR-499, and miR-21, in 102 patients with essential hypertension and 30 healthy individuals. All patients underwent two-dimensional echocardiography. MicroRNA expression levels in peripheral blood mononuclear cells were quantified by real-time reverse transcription polymerase chain reaction. Hypertensive patients showed significantly lower miR-133a (5.06 ± 0.50 vs. 13.20 ± 2.15, P < .001) and miR-26b (6.76 ± 0.53 vs. 9.36 ± 1.40, P = .037) and higher miR-1 (25.99 ± 3.07 vs. 12.28 ± 2.06, P = .019), miR-208b (22.29 ± 2.96 vs. 8.73 ± 1.59, P = .016), miR-499 (10.06 ± 1.05 vs. 5.70 ± 0.91, P = .033), and miR-21 (2.75 ± 0.15 vs. 1.82 ± 0.20, P = .002) expression levels compared with healthy controls. In hypertensive patients, we observed significant negative correlations of miR-1 (r = -0.374, P < .001) and miR-133a (r = -0.431, P < .001) and significant positive correlations of miR-26b (r = 0.302, P = .002), miR-208b (r = 0.426, P < .001), miR-499 (r = 0.433, P < .001) and miR-21 (r = 0.498, P < .001) expression levels with left ventricular mass index. Our data reveal that miR-1, miR-133a, miR-26b, miR-208b, miR-499, and miR-21 show distinct expression profiles in hypertensive patients relative to healthy individuals and they are associated with clinical indices of left ventricular hypertrophy in hypertensive patients. Thus, they may be related to heart hypertrophy in hypertensive patients and are possibly candidate therapeutic targets in hypertensive heart disease.

Early cardiac gene transcript levels in peripheral blood mononuclear cells reflect severity in stable coronary artery disease.

INTRODUCTION: The early cardiac marker genes myocardin, GATA4 and Nkx2.5, play a role in both embryonic cardiovascular development and adult cardiovascular disease. We evaluated transcript levels of myocardin, GATA4 and Nkx2.5 in peripheral blood mononuclear cells (PBMCs) in patients with stable coronary artery disease (CAD) and we examined the relationship between these levels and the severity of the disease, estimated by the number of stenotic vessels involved. METHODS: Ninety-eight patients with stable CAD (age 66 ± 9 years) who underwent coronary angiography participated in the study; 66 healthy individuals (age 58 ± 13 years) were also included for comparison. Gene transcript levels were determined by quantitative real-time reverse transcription polymerase chain reaction. RESULTS: Patients with 3-vessel CAD had elevated transcript levels of myocardin (median difference 2.7, p=0.001, 95% confidence interval, CI: 1-5.8), GATA4 (median difference 0.3, p=0.015, 95% CI: 0.1-1.9) and Nkx2.5 (median difference 16.1, p<0.001, 95% CI: 4.5-23) compared to healthy controls. Patients with 3-vessel CAD also showed elevated transcript levels of myocardin (median difference 2.3, p=0.001, 95% CI: 0.49-5.5) and Nkx2.5 (median difference 11.8, p<0.001, 95% CI: 1.5-21.5) compared to patients with 1-vessel CAD. CONCLUSIONS: Early cardiac marker gene transcript levels are significantly higher in the PBMCs of patients with severe stable CAD than in those of healthy controls, and show alterations in their expression profile according to the disease severity status. Our results indicate for the first time that changes in the early cardiac gene expression in the peripheral blood of stable CAD patients, possibly as a result of alterations in circulating cardiovascular progenitor cells that express these genes, may reflect the level of disease severity.

Association of sodium and potassium intake with ventricular arrhythmic burden in patients with essential hypertension.

BACKGROUND: Hypertensive populations suffer from an increased susceptibility to ventricular arrhythmias and sudden cardiac death. A high-salt diet appears to be a major factor involved in cardiovascular complications in hypertension. We examined the relationship between dietary salt and potassium, as indicated by urinary sodium (UNa), urinary potassium (UK), and urinary sodium/potassium ratio (UNa/K), and the arrhythmic burden in patients with essential hypertension. METHODS: We included 255 consecutive adult patients with well-controlled hypertension who were being followed in the hypertension outpatient clinic of a university tertiary hospital and complained of episodes of atypical chest pain and/or palpitations. All underwent 24-hour ambulatory electrocardiograph monitoring and their UNa, UK, and UNa/K ratio from 24-hour urinary excretion specimens were evaluated. RESULTS: No significant correlation was found between premature supraventricular contractions and the parameters that were examined. However, the percentage of premature ventricular contractions (PVC%) showed a weak positive association with UNa (r = 0.2; P = .001) and a moderate negative association with UK (r = -0.396; P < .001). The partial correlation coefficient of PVC% with the UNa/UK ratio remained significant even after controlling for left ventricular mass index (r = 0.437; P < .001). CONCLUSIONS: A higher UNa/UK excretion ratio is significantly associated with PVCs, indicating an increased susceptibility to ventricular arrhythmias even among hypertensives with well-controlled blood pressure. Our findings reinforce recommendations for dietary interventions in those populations.

Mechanisms, risk factors, and management of acquired long QT syndrome: a comprehensive review.

Long QT syndrome is characterized by prolongation of the corrected QT (QTc) interval on the surface electrocardiogram and is associated with precipitation of torsade de pointes (TdP), a polymorphic ventricular tachycardia that may cause sudden death. Acquired long QT syndrome describes pathologic excessive prolongation of the QT interval, upon exposure to an environmental stressor, with reversion back to normal following removal of the stressor. The most common environmental stressor in acquired long QT syndrome is drug therapy. Acquired long QT syndrome is an important issue for clinicians and a significant public health problem concerning the large number of drugs with this adverse effect with a potentially fatal outcome, the large number of patients exposed to these drugs, and our inability to predict the risk for a given individual. In this paper, we focus on mechanisms underlying QT prolongation, risk factors for torsades de pointes and describe the short- and long-term treatment of acquired long QT syndrome.

TLR2 and TLR4 gene expression in peripheral monocytes in nondiabetic hypertensive patients: the effect of intensive blood pressure-lowering.

The activation of innate immune receptors, such as Toll-like receptors (TLRs), participates in the pathogenesis of cardiovascular diseases. The authors evaluated TLR2 and TLR4 gene expression in the peripheral monocytes of nondiabetic hypertensive patients compared with normotensive individuals and investigated the effect of intensive systolic blood pressure (SBP)-lowering. Included were 43 nondiabetic hypertensive patients with essential hypertension who were randomly assigned to an intensive treatment arm, with an SBP target of <130 mm Hg, or a standard arm, with an SBP target of <140 mm Hg. TLR2 and TLR4 messenger RNA (mRNA) levels in monocytes were estimated before and 12 weeks after therapy initiation. Sixteen healthy individuals were included for comparison. Hypertensives revealed significantly higher TLR4 mRNA levels compared with normotensives (985 ± 885 vs 554 ± 234, P=.005). In contrast, no statistically significant difference was found in TLR2. Compared with standard treatment, intensive treatment significantly downregulated TLR2 and TLR4 mRNAs, expressed as fold induction (0.66 ± 0.49 vs 1.38 ± 1.65 and 0.62 ± 0.3 vs 1.9 ± 1.2, respectively; P<.001 for both). In conclusion, TLR4 mRNA levels in peripheral monocytes are significantly elevated in nondiabetic hypertensive patients. Intensive control of SBP results in attenuation of TLR2 and TLR4 gene expression in those patients. Our findings suggest that a strict SBP target in nondiabetic hypertensive patients may offer additional benefits.

Impact of Atrial Fibrillation on Coronary Blood Flow: A Systematic Review.

Patients with atrial fibrillation (AF) frequently present with symptoms suggestive of myocardial isch- aemia, even in the absence of significant CAD, that seem to be attributable to abnormalities of myocardial perfusion and perfusion reserve. According to the results of recent human and previous experimen- tal studies the increase in coronary artery blood flow during AF is smaller, while the coronary vascular resistance during the arrhythmia does not decrease as much as we would expect, suggesting a mismatch between coronary blood flow and myocardial metabolic demand. AF itself diminishes coronary flow reserve, especially in the subendocardial layer, partly as a result of the increase in the myocardial com- ponent of coronary vascular resistance, and it is possible that irregular ventricular rhythm may play an important role. The mismatch of coronary blood flow and myocardial metabolic demand, especially in view of the severe reduction in coronary flow reserve, may have deleterious consequences that are not limited to patients with CAD.

Differential effect of telmisartan and amlodipine on monocyte chemoattractant protein-1 and peroxisome proliferator-activated receptor-gamma gene expression in peripheral monocytes in patients with essential hypertension.

Monocyte chemoattractant protein-1 (MCP-1) and peroxisome proliferator-activated receptor-γ (PPAR-γ) play a significant role in monocyte activation, vascular inflammation, and atherogenesis. Angiotensin receptor blockers and calcium channel blockers are antihypertensive drugs with established efficacy and a favorable safety profile. We investigated the effect of telmisartan--an angiotensin receptor blocker with PPAR-γ agonist activity--and amlodipine on the activation state of peripheral blood monocytes with respect to MCP-1 and PPAR-γ gene expression in hypertensives. We recruited 31 previously untreated patients with essential hypertension who were randomly assigned to receive treatment with telmisartan (n = 16) or amlodipine (n = 15). Blood samples were taken before and 3 months after therapy initiation. Mononuclear cells were isolated and mRNAs of MCP-1 and PPAR-γ were estimated by real-time quantitative reverse transcription-polymerase chain reaction each time. The 2 treatments decreased all blood pressure components significantly (p <0.001). In contrast, in the amlodipine group, MCP-1 gene expression was significantly downregulated after treatment with telmisartan (from 21.4 ± 20.5 to 8.1 ± 6.5, p = 0.009), whereas the amlodipine group did not show any significant change (12.5 ± 8.5 vs 17.6 ± 16.4, p = NS). In addition, PPAR-γ mRNA levels showed a significant increase in telmisartan-treated patients (from 20 ± 18.5 to 42.6 ± 36, p = 0.006) and no significant alterations in the amlodipine group (from 29.6 ± 42.5 to 24.2 ± 27.7, p = NS). In conclusion, treatment with telmisartan results in a significant attenuation of MCP-1 gene expression and an increase of PPAR-γ gene expression in peripheral monocytes in patients with essential hypertension. Our findings may provide new insights into the cardiovascular protection of telmisartan in hypertensives.

Oxidative stress changes after stent implantation: a randomized comparative study of sirolimus-eluting and bare metal stents.

BACKGROUND: Although oxidative stress plays an important role in the pathophysiology of restenosis, its role following the implantation of sirolimus-eluting stents (SES) is unknown. METHODS: We examined the relation between total peroxides (TP), a marker of oxidative stress, and in-stent late luminal loss over a 6-month follow-up in patients with stable coronary artery disease and compared the results from SES with those from bare metal stents (BMS). We enrolled 75 consecutive patients, who underwent successful PCI and were randomly allocated to SES (n=37) or BMS (n=38). Blood samples were taken 24 h before, at 24 h, 48 h and 1 month after angioplasty; levels of TP were determined on each occasion. Follow-up coronary angiography was performed 6-8 months later. RESULTS: TP levels in the BMS group were significantly higher at 24 h and 48 h compared to baseline (p=0.006 for both). At one month there was a significant decline from the 48 h levels (p=0.029) to levels slightly, but not significantly higher than baseline. In contrast, in SES TP levels showed no significant changes during the first 48 h, while they declined to levels somewhat lower than baseline at 30 days. A significant correlation was found between TP changes and in-stent late luminal loss at 6 months in both groups. CONCLUSION: Our study showed that patients with stable coronary artery disease who received SES have a different behavior of oxidative stress after stenting compared with BMS, and this could contribute to the difference in restenosis rate between these 2 types of stents.

Right atrial myxoma: echocardiographic appearance.

A 67-year-old asymptomatic male was admitted for evaluation of his arterial hypertension. The routine echocardiographic study revealed a large tumour in the dilated right atrium. The mass appeared to arise from the posterior wall of the right atrium. After infusion of a contrast agent, the mass appeared to fill with the contrast agent, ruling out the possibility of the mass being a clot. Transesophageal study revealed a round mass arising from the posterior right atrial wall just adjacent to the extrusion of the superior vena cava. The patient subsequently underwent cardiac surgery and a cardiac tumour was excised that proved to be a cardiac myxoma. In this case we present echocardiographic images and the macro- and microscopic view of the right atrial myxoma.

Isolated atrial microvascular dysfunction in patients with lone recurrent atrial fibrillation.

OBJECTIVES: The purpose of this study was to assess atrial myocardial perfusion in patients with lone recurrent atrial fibrillation (LRAF). BACKGROUND: Although acute atrial ischemia has been implicated in the pathogenesis of atrial fibrillation, there are few data concerning human atrial myocardial perfusion and none for patients with LRAF. METHODS: Sixteen patients with LRAF and 15 control subjects with suitable coronary anatomy underwent time-averaged peak coronary blood flow velocity (APV) measurements (cm/s), using a Doppler guidewire in the proximal left circumflex coronary artery (LCx) and in the left atrial circumflex branch (LACB), at baseline (b) and after adenosine administration to achieve maximal hyperemia (h). Coronary flow reserve was defined as h-APV/b-APV. RESULTS: Although there were no statistically significant differences in b-APV between patients with LRAF and control subjects or between the LACB and LCx, there were significant group (p = 0.002), artery (p = 0.001), and interaction (p < 0.001) effects at maximal hyperemia. In patients with LRAF, the h-APV and coronary flow reserve of the LACB (30.4 +/- 9.5 cm/s and 2.2 +/- 0.4, respectively) were significantly lower than in the LACB of the control subjects (45.8 +/- 12.8 cm/s [p < 0.001] and 2.9 +/- 0.5 [p = 0.001], respectively) or in the patients' LCx (43.0 +/- 10.9 cm/s [p = 0.001] and 3.1 +/- 0.6 [p < 0.001], respectively). CONCLUSIONS: This study confirms for the first time isolated atrial myocardial perfusion abnormalities in patients with LRAF and coronary flow reserve impairment, indicating that microvascular dysfunction is a pathophysiological substrate associated with this arrhythmia.

Vascular endothelial growth factor protein levels and gene expression in peripheral monocytes after stenting: a randomized comparative study of sirolimus: eluting and bare metal stents.

AIMS: Although previous studies have indicated that vascular endothelial growth factor (VEGF) plays an important role in the vascular-healing process after stent implantation, its effect on in-stent restenosis is unclear. We assessed VEGF serum protein levels and gene expression in peripheral monocytes in relation to in-stent restenosis after implantation of sirolimus-eluting (SES) and bare metal stents (BMS) in a non-blinded, randomized study. METHODS AND RESULTS: Forty-two patients (28 men, age 62 +/- 11 years) with stable angina, who underwent elective single-vessel percutaneous coronary intervention, were randomized to SES (n = 21) or BMS (n = 21) implantation. VEGF protein levels in the BMS group showed an increasing trend (P = 0.083), whereas in the SES group they decreased significantly (P = 0.002). BMS induced up-regulation of VEGF mRNA levels, whereas for SES down-regulation was observed. There was no correlation between serum levels and late luminal loss. A significant correlation was found between VEGF gene expression and late luminal loss in both groups (BMS: r = 0.98, P < 0.001; SES: r = 0.65, P = 0.002). CONCLUSION: SES, in comparison with BMS, results in lower VEGF protein levels and gene expression in peripheral monocytes. The latter shows a positive relationship with in-stent late-luminal loss, suggesting an essential role in the reduced in-stent restenosis seen in SES.

Acute effect of esmolol intravenously on coronary microcirculation in patients with idiopathic dilated cardiomyopathy.

Although coronary flow reserve (CFR) impairment was correlated with the prognosis of patients with idiopathic dilated cardiomyopathy (IDC) and microvascular ischemia was implicated in the progress of the disease, little is known about the effect of the established therapy with beta blockers on coronary microcirculation. The purpose of this study was to assess the effect of beta(1) blockade on coronary blood flow and CFR in patients with IDC. Fourteen patients with IDC and 10 control subjects underwent time-averaged peak coronary flow velocity (APCFV) measurements (centimeters per second) in the proximal left anterior descending coronary artery at baseline and at maximal hyperemia before and after beta(1) blockade with intravenous esmolol. CFR was defined as APCFV at maximal hyperemia/APCFV at baseline. Although there were no significant differences in APCFV at baseline between patients with IDC and controls, patients with IDC had significantly lower APCFV at maximal hyperemia than controls (54.2 +/- 12.0 vs 75.1 +/- 18.6, p <0.05) and decreased CFR (2.39 +/- 0.38 vs 3.50 +/- 0.54, respectively, p <0.05). After beta(1) blockade, a significant decrease in APCFV at baseline (19.5 +/- 3.7 vs 22.9 +/- 5.0, p <0.05) and enhancement of APCFV at maximal hyperemia (59.5 +/- 13.3 vs 54.2 +/- 12.0, p <0.05) were observed in patients with IDC, but not in control subjects, leading to significant improvement in CFR (3.06 +/- 0.40 vs 2.39 +/- 0.38, p <0.05). In conclusion, patients with IDC had alterations in coronary blood flow and decreased CFR that improved after beta(1) blockade. These alterations in microvascular function, which are partially reversed by beta blockade, may be 1 of the underlying mechanisms that contribute to the improved prognosis of patients with IDC under such therapy.

A comparative study of the efficacy and safety of procainamide versus propafenone versus amiodarone for the conversion of recent-onset atrial fibrillation.

The appropriate treatment for the restoration of sinus rhythm in patients with atrial fibrillation (AF) of recent onset is still the subject of controversy. In this prospective, randomized, single-blind, placebo-controlled clinical study, we investigated the effectiveness and safety of procainamide, propafenone, and amiodarone, administered intravenously, for the conversion of recent-onset AF. We enrolled 362 consecutive patients (183 men; age 34 to 86 years; mean 65+/-10) with AF duration of no >48 hours. Of these patients, 89 were given procainamide, 91 propafenone, 92 amiodarone, and 90 placebo. Treatment was considered successful if conversion to sinus rhythm was achieved within the 24-hour study period. Baseline clinical characteristics were similar in the 4 groups. The treatment was successful in 61 of the 89 patients who received procainamide (68.53%; median time 3 hours), 73 of the 91 patients who received propafenone (80.21%; median time 1 hour), 82 of the 92 patients who received amiodarone (89.13%; median time 9 hours), and 55 of the 90 patients who received placebo (61.11%; median time 17 hours; p<0.05 for all medicated groups vs placebo; p<0.05 for amiodarone and propafenone vs procainamide). In conclusion, all 3 medications, when administered intravenously, are effective in the restoration of sinus rhythm in recent-onset AF. Amiodarone and propafenone are more effective whereas procainamide and propafenone are faster.

Combined use of aspiration catheter and distal embolisation protection device to facilitate angioplasty of a totally occluded saphenous vein graft.

Angioplasty of totally occluded saphenous vein grafts is a very challenging procedure and the likelihood of distal embolisation and no-reflow is much higher than in any conventional angioplasty. The use of thrombus aspiration and distal protection devices, although not well studied in a large number of patients, has been shown to be quite effective in preventing such complications. In this case we report our satisfactory experience from the combined use of a novel aspiration catheter and a distal protection device for the treatment of a totally occluded saphenous vein graft.

Acute coronary syndrome in an adult with anomalous origin of the left anterior descending coronary artery from the pulmonary trunk.

Anomalous origin of the left anterior descending coronary artery is a very rare coronary vascular anomaly, especially in adults. We describe the case of a 45-year-old woman who presented with an acute coronary syndrome. Coronary angiography revealed an anomalous origin of the left anterior descending coronary artery from the main pulmonary trunk, with collateral filling from both the left circumflex and the right coronary artery. Treatment of choice of this coronary anomaly is usually surgical repair, while intense antithrombotic therapy should be considered, especially if the anomalous vessel is ectatic.

Effect of inhaled salbutamol on coronary circulation in humans.

In 12 patients we assessed the effect of inhaled salbutamol on the coronary circulation. According to our results, large doses of salbutamol increase coronary flow, but not in proportion to the needs of the myocardium (as documented by the increase in coronary oxygen extraction), and decrease coronary flow reserve. These effects may have deleterious consequences in patients with coronary artery disease, causing or worsening myocardial ischemia.