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Historically, in high-risk patients with cardiovascular disease, anticoagulants have been used in order to reduce the risk of stroke or other ischemic complications. However, despite this seemingly simple solution, drug selection and dosage control may provide a unique challenge when it comes to the anticoagulation therapy of individual patients. In this case report, a patient with multiple underlying conditions and two previous stroke episodes was admitted due to decompensated heart failure and was treated with anticoagulants to reduce the risk of developing secondary stroke(s). The initially prescribed anticoagulative agent, acenocoumarol, was discontinued and subsequently replaced with enoxaparin due to unstable INR and undiagnosed anaemia. Unfortunately, newer anticoagulants were contraindicated in this patient due to the previous implantation of the mechanical aortic valve. This study reveals and discusses the conundrum faced in prescribing anticoagulants to patients with multiple conditions of underlying diseases. Despite the aforementioned hurdles, anticoagulant therapy in these patients is crucial in avoiding potential life-threatening complications, including myocardial infarction and secondary stroke; proper prescription decisions may ultimately decrease morbidity and improve the quality of life of these high-risk patients.

Left ventricular (LV) systolic function is often measured with echocardiography using LV ejection fraction (LVEF) or global longitudinal peak systolic strain (GLPSS). Global wasted work (GWW), global work efficiency (GWE), and first-phase ejection fraction (LVEF-1) are newer LV systolic function indices. We examined these parameters in 45 healthy individuals and 50 patients with stable coronary artery disease (CAD), normal LV contractility, and LVEF > 50%. Compared to healthy individuals, CAD patients had similar LVEF but increased GLPSS and GWW and reduced GWE and LVEF-1. The highest area under the receiver operating characteristic for detecting CAD was found for LVEF-1 (0.84; 95% CI 0.75–0.91; p < 0.0001), and it was significantly larger than for GLPSS (+0.166, p = 0.0082) and LVEF (+0.283, p = 00001). For LVEF-1 < 30%, the odds ratio for the presence of CAD was 22.67 (95% CI 6.47–79.44, p < 0.0001) in the logistic regression adjusted for age, sex, and body mass index. Finding LVEF-1 < 30% in an individual with normal LV myocardial contraction and preserved LVEF strongly suggests the presence of CAD.

Autorzy przedstawiają z perspektywy długoletniej praktyki lekarskiej poglądy Władysława Szenajcha (1879-1964), pediatry, filozofa medycyny i społecznika, na powinności etyczne lekarza. W artykule znajduje się biogram Stanisława Obrębowskiego.

INTRODUCTION Grip strength and blood pressure are strongly interrelated. Blood pressure is an essential component of arterial load, which modulates cardiac output. OBJECTIVES We aimed to asses the correlation between grip strength and both steady and pulsatile components of arterial load in patients with acute myocardial infarction. PATIENTS AND METHODS We included 295 participants (mean age, 63 years) with acute myocardial infarction. The following data were assessed: grip strength, echocardiography, local arterial stiffness, arterial tonometry, continuous arterial pulse, and beat‑to‑beat wave. RESULTS In univariable analyses, grip strength correlated with arterial stiffness (pulse wave velocity), ventricular-arterial coupling, and measures of pulsatile arterial load: aortic characteristic impedance (Zao), total arterial compliance (TAC), and central fractional arterial pulse pressure (cFPP). In a multivariable model including age, grip strength, body mass index, systolic blood pressure, sex, and descriptors of pulsatile load, the following remained associated with grip strength: Zao (R2 for the model = 0.58; P

Objectives. Reduced muscular strength (measured by grip strength) has been associated with an increased risk of cardiovascular complications. Further research is needed to identify how muscular str...

Background . During myocardial ischemia, activation of polymorphonuclear neutrophils (PMNs) results in the production of free oxygen radicals, which increase myocardial injury. It has been shown that PMNs also produce nitric oxide. It is not clear whether PMNs become activated as a result of their direct contact with ischemic/reperfused myocardium or if PMN activation and free oxygen radical production are effects of specific stimuli released during coronary artery bypass grafting (CABG). The aim of the current study was to evaluate plasma-mediated neutrophil stimulation and production of superoxide anion (O 2 ) and nitric oxide in patients undergoing CABG, and to verify whether crystalloid and blood cardioplegia can modify such stimulation. Methods . Coronary sinus, peripheral arterial, and venous plasma samples were collected from 50 patients who underwent CABG and were divided into 2 equal groups which received either crystalloid or blood cardioplegia: directly before myocardial ischemia and aortic cross-clamping; at the beginning of reperfusion after aortic clamp release; and 30 minutes after reperfusion. O 2 and nitric oxide production by PMN was evaluated by standard methods. Results . There was a significant ( p 2 production by PMN incubated with plasma obtained from the coronary sinus immediately after reperfusion in patients receiving crystalloid cardioplegia compared to blood cardioplegia. No difference was observed in plasma stimulation of nitric oxide production by PMN in the 2 groups of patients at different times during the procedure. Conclusions . Cardioplegia may affect release of neutrophil-oriented stimuli from ischemic myocardium and modify neutrophil activation during coronary artery bypass grafting.

Myocardial ischemia leads to the activation of neutrophils as well as endothelial cells. The interaction between these cells is dependent on certain adhesion glycoproteins which are expressed on their surface. Adhesion of neutrophils to endothelium, mediated by adhesion molecules, has been shown to result in coronary capillary plugging and impairment of coronary blood flow. In certain conditions, upon cell activation, adhesion proteins may be released in soluble form into the circulating blood. The purpose of our study was to verify whether myocardial ischemia occurring during angina episodes results in the release of the soluble adhesion molecules, L-selectin, E-selectin, and intracellular adhesion molecule-1 (ICAM-1), into the circulation. Plasma samples were collected by venepuncture from 15 patients admitted to the emergency room with chest pain caused by attacks of angina pectoris and 15 patients with noncardiac chest pain. To confirm the diagnosis, all patients underwent an exercise stress test and, if not conclusive, 99mTc MIBI SPECT or coronary arteriography. Another set of plasma samples were taken from each patient in the absence of chest pain. In addition, blood for analysis was obtained from 15 sex-and age-matched healthy subjects. Soluble adhesion molecules plasma levels were measured by standard enzyme-linked immunosorbent assay. In patients with angina pectoris, plasma levels of soluble L-selectin estimated during chest pain were significantly higher than in the control group and decreased in the absence of chest pain. Similarly, the mean concentration of soluble ICAM-1 at the time of angina onset was significantly elevated in the patients in comparison with the control group and remained higher, although not significantly, in the absence of chest pain. In patients with noncardiac chest pain, plasma levels of soluble L-selectin did not differ significantly from those observed in control subjects. In this group of patients, the plasma levels of soluble ICAM-1 estimated during pain onset and in the absence of this symptom were not significantly elevated. On the contrary, the mean values of soluble E-selectin in the patients with ischemic cardiac pain during chest pain and in the absence of this symptom, as well as those in the patients with noncardiac chest pain during or without symptoms, remained unchanged in comparison with the control group. During attacks of angina pectoris an increase in the plasma levels of the soluble adhesion molecules, ICAM-1 and L-selectin, was noted, possibly reflecting activation of neutrophils and endothelial cells during myocardial ischemia. However, E-selectin plasma levels remained unchanged in response to myocardial ischemia.

Typical chest pain and ECG changes suggest the presence of myocardial ischaemia in cardiac syndrome X (SX) patients and resemble the symptoms observed in subjects with atherosclerotic coronary artery disease (CAD).To compare the results of exercise treadmill tests (ETT), 24-hour ECG recordings and echocardiography in SX and CAD patients without previous myocardial infarction with the presence of significant lumen stenosis in one (CA1), two (CA2) or three (CA3) coronary arteries.Two hundred six patients were included in the study: 43 SX (28 female), 49 CA1 (11 female), 51 CA2 (7 female) and 63 CA3 patients (8 female) all of whom underwent ETT according to the Bruce protocol, 24-hour ECG recordings and echocardiography.SX patients had median ST-segment depression during ETT comparable to that in CA1 and CA2 patients but significantly less than the CA3 subjects (p=0.024). Median time to ST depression of at least 1 mm, as well as median time of exercise, was significantly longer in SX individuals than in all CAD patients. The post-exercise recovery time of ST-segment changes was significantly longer in SX patients than in the CA1 group (p=0.006), comparable to that in CA2 subjects and shorter than that in CA3 individuals (p=0.003). Both the maximal ST-segment depression and the duration of significant ST-segment depression in Holter ECG recordings were significantly higher in SX patients than in CA1 subjects, were comparable to the values observed in the CA2 group and significantly lower than in CA3 individuals. The heart rate variability parameters (SDNN and pNN50) were significantly higher in SX patients than in CAD subjects. Patients with SX had a significantly thinner interventricular septum and smaller left ventricular end-diastolic cavity dimension than individuals from the CA1, CA2 and CA3 groups. There were no significant differences in the left ventricular ejection fraction or the thickness of the left ventricular posterior wall between SX patients and CAD patients.Analysis of the ST segment in SX patients suggests the presence of advanced CAD. However, SX patients have better heart rate variability and exercise performance than patients with CAD.

Several hemodynamic indices, measured invasively in the ascending aorta during routine angiography, are related to the presence and severity of coronary atherosclerosis. Radial artery tonometry, when combined with a validated transfer function, offers the possibility of noninvasive assessment of central arterial pressure. We aim to evaluate the association between noninvasive indices of aortic or radial pressure waveforms and the presence of a significant coronary stenosis. Patients who underwent elective coronary angiography were studied (110 men, 91 women, mean age 53 +/- 0.9 years). Noninvasive measurement of their central hemodynamics was performed by analysis of the aortic pressure waveform derived from the radial artery. An increase in aortic fractional pulse pressure was associated with coronary artery narrowing or previous myocardial infarction. After multivariate adjustment, the odds ratio and confidence intervals (CI) of having a significant coronary aortic stenosis was 1.72 (95% CI, 1.1-2.7) and of previous myocardial infarction 1.6 (95% CI, 1.1-2.2). An increase in noninvasively assessed aortic fractional pulse pressure, but not of the peripheral index is significantly associated with the presence of coronary artery disease.