Implications of Myocardial Bridge on Coronary Atherosclerosis and Survival.

Background: In this study, we aimed to describe the impact of MBs on atherosclerosis and survival, in patients with coronary artery disease (CAD). Methods: We retrospectively studied 1920 consecutive patients who underwent conventional coronary angiography for suspected CAD. Atherosclerotic load (AL), defined as the sum of degrees of stenosis, and general atherosclerotic load (GAL), representing the sum of AL, were compared between patients with MB and a control group without MB; patients in these groups were similar in age and sex. We assessed survival at 10 years after the last enrolled patient. Results: Prevalence of MB was 3.96%, predominantly in the mid-segment of left anterior descendent artery (LAD). In the presence of MB, GAL was lower (158.1 ± 93.7 vs. 205.3 ± 117.9, p = 0.004) with a lesser AL in the proximal (30.3 ± 39.9 vs. 42.9 ± 41.1, p = 0.038) and mid-segments (8.1 ± 20.0 vs. 25.3 ± 35.9, p < 0.001) of LAD. Based on a Multinominal Logistic Regression, we found that the presence of MB on LAD (regardless of its location on this artery) is a protective factor against atherosclerotic lesions, decreasing the probability of significant stenosis, especially of those ≥70%, on the entire artery (B −1.539, OR 4660; 95% CI = 1.873−11.595, p = 0.001) and on each of its segments as well: proximal LAD (B −1.275, OR 0.280; 95% CI = 0.015−5.073; p = 0.038), mid-LAD (B −1.879, OR 6.545; 95% CI = 1.492−28.712; p = 0.013) and distal LAD (B −0.900, OR 2.459, 95% CI = 2.459−2.459, p = 0.032). However, 10-year survival was similar between groups (76.70% vs. 74.30%, p = 0.740). Conclusion: The presence of MB on LAD proved to be a protective factor against atherosclerosis for the entire artery and for each of its segments, but it does not influence long-term survival in patients with CAD.

Therapeutic Challenges in Patients With Noncardioembolic Acute Ischemic Stroke in Need of Double Antiplatelet Therapy for Coronary Artery Disease.

BACKGROUND: The risk of ischemic stroke (IS) is significant within 6-12 months from the myocardial revascularization for an acute cardiac event. Consequently, we can expect to have patients with an acute IS occurring right in the time frame of dual antiplatelet therapy (DAPT) imposed by the coronary heart disease (CHD). AREAS OF UNCERTAINTY: Until present, there are no evidence-based guidelines for the management of patients with acute IS in need of DAPT for ischemic heart disease. The aim of this article was to go through the available data and to depict the appropriate therapeutic strategy for this category of patients. DATA SOURCES: We have performed a systematic review of the literature through June 2018, using Medline/PubMed database. THERAPEUTIC ADVANCES: DAPT (aspirin and only clopidogrel among all P2Y12 inhibitors) might be maintained or initiated for CHD in patients with minor acute stroke and high-risk transient ischemic attack patient with IS attributable to an important intracranial stenosis, as long as this drug combination proved to be safe for them in the prevention of stroke recurrence. In patients with IS receiving thrombolysis, with increased size of infarction or high National Institute of Health Stroke Score (NIHSS), the risk of hemorrhagic transformation under DAPT must be weighed against the risk of stent thrombosis in the coronary arteries, which, on its turn, depends on the clinical form for which myocardial revascularization was performed, the time interval from the complexity of a certain interventional procedure. CONCLUSIONS: In the acute phase of an IS, maintenance or initiation of DAPT therapy imposed by CHD relies, on one hand, on the risk of hemorrhagic transformation of the brain injury and, on the other hand, on the risk of stent thrombosis in the coronary arteries. The management of these patients must be carried on by a vascular team, on an individualized basis.

Advanced Atherosclerosis with Leriche Syndrome, in a Patient with Carney Complex.

Carney complex (CNC) is a rare autosomal dominant syndrome. Spotty skin pigmentation is the major clinical manifestation of CNC, followed by cardiac myxomas, benign tumors that usually present with features from the classical triad of obstructive cardiac, embolic and non-specific constitutional symptoms (NCS). NCS are caused by the overproduction of interleukin-6 (IL-6), a pro-inflammatory cytokine which mediates the induction of intercellular adhesion molecule 1 (ICAM-1) and promotes endothelial dysfunction and atherosclerosis. Thus, myxomas may be directly linked to an increased risk of atherosclerotic events. We report here a case of a 74-year-old woman with left atrial myxoma, skin pigmentary abnormalities, thyroid disorder and extensive atherosclerosis, with non-embolic occlusion of infrarenal abdominal aorta.

Acute Myocardial Injury in a Child with Duchenne Muscular Dystrophy: Pulse Steroid Therapy?

Heart implication in Duchenne muscular dystrophy usually is present in the form of dilated cardiomyopathy, manifested as heart failure and arrhythmias. To delay progression, including heart deterioration, prednisone is recommended as preventive treatment. We report the case of an 11-year-old boy diagnosed with Duchenne muscular dystrophy at the age of seven, who was on preventive treatment with oral prednisone (0.75 mg/kg/day) and beta blocker (metoprolol, 1 mg/kg/day). Suddenly, the patient presented acute chest pain, vomiting and sweating. The electrocardiogram showed ST elevation in inferior leads. Troponin T was increased to 30814 pg/ml (normal values <14 pg/mL). The echocardiography revealed reduced contractility of the posteroinferior wall of the left ventricle. After excluding coronary implications by coronary angiography, we increased the oral prednisone to 1.4 mg/kg/day for five days and added enalapril (0.5 mg/kg/day, po). The response was positive, with a rapid decrease of the troponin T value to 3186 pg/mL in five days and gradual recovery of myocardial contractility afterwards.

Arterial Stiffness and Hypertension - Which Comes First?

Arterial hypertension is one of the traditional risk factors involved in the development of cardiovascular events, while arterial stiffness is an independent predictor of cardiovascular disease in patients with hypertension. It seems that the risk factors involved in the pathology of uncontrolled hypertension are similar to those that contribute to the development of arterial stiffness. After evidence showed that arterial stiffness is an independent prognostic factor for the occurrence of cardiovascular events in patients with arterial hypertension, the importance of assessing arterial stiffness was recognized in a document drafted by the European Society of Hypertension in 2007. Many factors, some still insufficiently studied, are involved in the development and worsening of arterial stiffness, especially in patients with certain comorbidities (diabetes, hypertension, chronic kidney disease). The evaluation of pulse wave velocity (PWV) remains the gold standard for non-invasive assessment of arterial stiffness. It seems that changes in terms of lifestyle and drug therapy have some positive effects on improving arterial stiffness, but further studies are needed to prove this concept. Our review aims to highlight the novelty of the mechanisms, the assessment methods, some of the clinical aspects, as well as the therapeutic implications of arterial stiffness, especially in patients with hypertension.

Predictors of in-Hospital Mortality of ST-Segment Elevation Myocardial Infarction Patients Undergoing Interventional Treatment. An Analysis of Data from the RO-STEMI Registry.

BACKGROUND: ST-segment elevation myocardial infarction (STEMI) remains a leading cause of morbidity and mortality worldwide. Primary percutaneous coronary intervention (pPCI) is the preferred therapy for STEMI if it is done within 120 min from the first medical contact, by an experienced team in a high-volume center. The aim of this study was to assess the clinical characteristics and predictors of in-hospital mortality of patients with STEMI treated by percutaneous coronary interventions (PCIs). METHODS: We analyzed data from 15,076 STEMI patients enrolled in the RO-STEMI registry (ROmanian ST-Elevation Myocardial Infarction registry). Patients were divided into 2 groups: PCI (11.669; 77%) and conservative treated (3.407; 23%). PCI group includes both pPCI treated patients (84.3%), and patients undergoing rescue PCI (6.4%) and late PCI (9.3%). RESULTS: The mean age of STEMI patients was 62.7+/-12.7 years. 70% were males. Patients treated by PCI were younger (61.4+/-12.2 versus 67.2+/-13.3, p< 0.0001) and more often men (80% versus 71%, p< 0.0001). They were less likely to have acute heart failure (Killip class II-IV) at admission (p< 0.0001). During admission, patients treated by PCI received more often dual antiplatelet therapy (97.6% versus 90.8%, p< 0.0001), statins (96.3% versus 87.5%, p< 0.0001), beta-blockers (83.8% versus 73.2%, p< 0.0001), and RAAS blockers (82.6% versus 66.4%, p< 0.0001). Overall in-hospital mortality was 7.1%: 4.1% in the PCI group and 15.7% in the conservative treated group. Multivariate analysis showed that, after adjusting for all clinical variables, Killip class II-IV at admission (OR: 9.2; 95%CI: 6.2-13.6; p< 0.0001), LVEF< 35% (OR: 3.8; 95%CI: 2.6-5.4; p< 0.0001), age older than 65 years (OR: 2.2; 95%CI: 1.5-3.2; p< 0.0001), and anterior location of myocardial infarction (OR: 2.1; 95% CI: 1.5-3; p< 0.0001) remained independent predictors for in-hospital mortality for STEMI patients treated interventionally. CONCLUSION: Advanced Killip class, depressed LVEF, advanced age, and anterior location were the most powerful independent predictors of in-hospital mortality in STEMI patients who underwent interventional treatment.

Outcome and Predictors of Stent Thrombosis in the First Romanian Registry of Drug Eluting Stent (RODESINO EXTENSION).

BACKGROUND: Stent thrombosis (ST) is a rare, but extremely severe complication of PCI. Outside clinical trials, data are limited regarding the risks and the impact of this phenomenon. AIMS: To assess prevalence, predictors, and clinical outcome of ST after implantation of drug eluting stents (DES) compared with bare metal stents (BMS), in a large case-control study in a real world scenario, as well as the relation between ST and duration of combined antiplatelet treatment. METHODS: In a case-control registry we included 475 patients who received at least 1 DES (sirolimus, zotarolimus, everolimus, paclitaxel), compared with a group of 475 patients who received at least 1 BMS. We used 1.22 DES/patient vs. 1.26 BMS/patient (p=ns), treating 1.02 DES/lesion vs. 1.05 BMS/lesion (p=ns). Main outcome was ST defined by the Academic Research Consortium (ARC) as definite (acute, sub-acute, late), probable, and possible. RESULTS: At 15 months we found 0.8% (4) patients in the DES group vs. 1.1% (5) patients in the BMS group with definite ST (ns); 0.4% (2) patients from each group had acute ST, while 0.4% (2) vs. 0.7% (3) patients had sub-acute ST (both comparisons were ns). None of the patients from the DES group died, whereas two patients with definite ST from the BMS group died, with a case fatality rate of 40% (2/5). 0.2% (1) patient from each group had probable ST (ns) and 0.6% (3) vs. 0.4% (2) patients had possible ST (ns). Independent predictors of stent thrombosis in merged groups were antiplatelet therapy discontinuation (HR 3.8; 95%CI 1.9-7.6; p<0.01), diabetes (HR 2.15; 95%CI 1.4-5.1; p<0.01), a lower left ventricular ejection fraction (EF) (HR 1.1; 95%CI 1.0-1.9; p<0.01 for each 10% decrease), and LAD lesions (HR 1.0; 95%CI, 0.93-1.9; P<0.01). CONCLUSIONS: ST is a rare complication (0.95%), similar after DES or BMS implantation. Premature discontinuation of antiplatelet therapy, followed by diabetes and a lower LVEF, are the independent predictors of ST.

"Supranormal" cardiac function in athletes related to better arterial and endothelial function.

OBJECTIVE: Athlete's heart is associated with left ventricular (LV) hypertrophy (LVH), and "supranormal" cardiac function, suggesting that this is a physiological process. Hypertrophy alone cannot explain increase in cardiac function, therefore, other mechanisms, such as better ventriculo-arterial coupling might be involved. METHODS: We studied 60 male (21 +/- 3 years) subjects: 27 endurance athletes, and a control group of 33 age-matched sedentary subjects. We assessed global systolic and diastolic LV function, short- and long-axis myocardial velocities, arterial structure and function and ventriculo-arterial coupling, endothelial function by flow-mediated dilatation, and amino-terminal pro-brain natriuretic peptide (NT-proBNP) and biological markers of myocardial fibrosis and of oxidative stress. RESULTS: Athletes had "supranormal" LV longitudinal function (12.4 +/- 1.0 vs 10.1 +/- 1.4 cm/s for longitudinal systolic velocity, and 17.4 +/- 2.6 vs 15.1 +/- 2.4 cm/s for longitudinal early diastolic velocity, both P < 0.01), whereas ejection fraction and short-axis function were similar to controls. Meanwhile, they had better endothelial function (16.7 +/- 7.0 vs 13.3 +/- 5.3%, P < 0.05) and lower arterial stiffness (pulse wave velocity 7.1 +/- 0.6 vs 8.8 +/- 1.1 m/s, P = 0.0001), related to lower oxidative stress (0.259 +/- 0.71 vs 0.428 +/- 0.88 nmol/mL, P = 0.0001), with improved ventriculo-arterial coupling (37.1 +/- 21.5 vs 15.5 +/- 13.4 mmHg.m/s(3)x 10(3), P = 0.0001). NT-proBNP and markers of myocardial fibrosis were not different from controls. LV longitudinal function was directly related to ventriculo-arterial coupling, and inversely related to arterial stiffness and to oxidative stress. CONCLUSIONS: "Supranormal" cardiac function in athletes is due to better endothelial and arterial function, related to lower oxidative stress, with optimized ventriculo-arterial coupling; athlete's heart is purely a physiological phenomenon, associated with "supranormal" cardiac function, and there are no markers of myocardial fibrosis.