Articles

This is demonstration of selected ECGs for learning or for exams; guided by lessons from great teachers as Prof. Hein Wellens MD. Here we provide advanced examples with comment and analysis.

This is a review of features in ECG to diagnose the culprit artery responsible for the infarction. Localization of the occluded vessel in acute myocardial infarction is important for many reasons: to know which artery is to dilate and stent; to assess the severity of the lesion; to compare with the echocardiographic area with hypokinesia or akinesia and to differentiate the recent from the old occluded vessel. The ST-segment changes in 12-lead ECG form the basis of diagnosis, management, and prognosis.

The involvement of the angiotensin II type 1 receptor in the Frank-Starling Law of the Heart, where the various activations are very limited, allows simple analysis of the kinase systems involved and thence extrapolation of the mechanism to that of angiotensin control of activation of cardiac and skeletal muscle contraction. The involvement of phosphorylation of the myosin light chain in the control of contraction is accepted but not fully understood. The involvement of troponin-I phosphorylation is also indicated but of unknown mechanism. There is no known signal for activation of myosin light chain kinase or Protein Kinase C-βII other than Ca2+/calmodulin but the former is constitutively active and thus has to be under control of a regulated inhibitor, the latter kinase may also be the same. Ca2+/calmodulin is not activated in Frank-Starling, i.e. there are no diastolic or systolic [Ca2+] changes. I suggest here that the regulated inhibition is by myosin light chain phosphatase and/or β-arrestin. Angiotensin activation, not involving G proteins. is by translocation of the β-arrestin from the sarcoplasm to the plasma membrane thus reducing its kinase inhibition action in the sarcoplasm. This reduced inhibition has been wrongly attributed to a mythical downstream agonist property of β-arrestin.

Purpose: There are uncertainties about whether general or central obesity is the more important determinant for blood pressure and hypertension in young Chinese. We aim to investigate the association between adiposity measures and blood pressure and hypertension in young medical students. Methods: A total of 380 medical students were recruited from the 2012 batch in the Clinical College of Dali University. Anthropometric measures and office blood pressure were measured. Blood pressure status was defined by Chinese hypertension guidelines and ACC/AHA 2017 hypertension guidelines, respectively. We examined the associations of adiposity measures (body weight, body mass index [BMI], waist circumference, hip circumference, waist-to-hip ratio [WHR], waist-to-height ratio [WHtR], ponderal index [PI], body adiposity index (BAI) and conicity index [CI]) with blood pressure and hypertension by sex. Results: In 380 subjects (women 66.6%, mean age 21.5 years), the prevalence of obesity (BMI ≥ 28 kg/m2) was 2.1%, and the prevalence of hypertension was 2.6% (≥ 140/90 mmHg) and 24.5% (≥ 130/80 mmHg), respectively. In correlation analyses and multivariable-adjusted linear regression analyses, most adiposity measures of central obesity were significantly associated with blood pressure in men, while in women, either adiposity measures of central or general obesity were associated with blood pressure. The predictive power of adiposity measures for hypertension was generally low in men. However, adiposity measures of either general obesity or central obesity were predictive for hypertension defined by Chinese hypertension guidelines in women. Conclusion: There are gender-specific associations of central and general obesity with blood pressure and hypertension in young Chinese medical students.

Permanent pacemaker implantation is conventionally done via upper limb veins. But in 1% - 6% cases, usual sub clavicular approach is either not possible or contraindicated due to complete occlusion of superior vena cava (SVC) or bilateral subclavian vein and/or bilateral implant site infection or thin skin [1]. Alternative approaches are warranted, including leadless pacemaker or complex lead extraction techniques, before considering surgical epicardial lead placement as a last resort because it has own hazards. We report a patient with complete heart block, total SVC obstruction, and a previously implanted malfunctioning epicardial lead presenting with pacemaker end of life. In view of exhaustion of the surgical option and in a resource constrained situation for lead extraction or leadless pacemaker, transiliac endocardial pacemaker implantation was done and a repeat surgery was averted. Learning objective: Complete venous occlusion is not very often encountered after pacemaker/ICD implantation. Apart from the risk of general anesthesia and invasive surgery, epicardial leads increase battery drain, and have a shorter operating life compared to an endocardial lead. The sparingly utilized iliac venous approach for permanent pacemaker implantation is a valuable, safe and minimally invasive alternative, when the conventional percutaneous access is unavailable, and surgery is undesirable or not possible. 

A 60-year-old female patient presented with typical anginal pain on exertion and relieved by rest for about one month. Percutaneous coronary angiography was done and showed an abnormal left circumflex coronary artery connecting to intercostal artery. Embolization of that abnormal connection was done successfully and the patient discharged from hospital after 24 hours. This case shows a new form of coronary steal syndrome. This cause could be missed if not put under the differential diagnosis of typical anginal pain with normal coronary arteries.

Background: Inflammation is associated with enhanced cardiovascular risk profile and increased cardiovascular mortality in end-stage kidney disease patients undergoing hemodialysis. Mechanisms of activated acute phase reaction in patients on chronic hemodialysis remain to be identified. As successful treatment of the inflammatory condition in these patients may improve long-term survival, we studied potential changes in different inflammatory biomarkers of cardiovascular risk in end-stage kidney disease patients after a mid-week hemodialysis session. Methods: Inflammatory biomarkers of cardiovascular risk (cystatin-C, homocysteine, C-reactive protein, procalcitonin, pentraxin-3, serum amyloid-A) and atherogenic plasma lipoproteins (Lipoprotein(a), cholesterol low and high density lipoproteins) were studied in 21 end-stage kidney disease patients previously and after a mid-week hemodialysis session. Results: We found a significant reduction in serum levels of low molecular weight molecules: cystatin-C (5.56 to 1.85 mg/L, 66.73%, p < 0.001), homocysteine (22.85 to 13.25 µmol/L, 42.01%, p < 0.001) and procalcitonin (0.788 to 0.457 ng/mL, 42.01%, p < 0.001). Large molecules as C-reactive protein (9.70 to 9.90 mg/L, 2.06%, p = 0.022) and pentraxin-3 (1.67 to 4.28 ng/mL, 156%, p < 0.001) increased, but serum amyloid-A decreased (15.90 to 12.70 mg/L, 20.13%, p < 0.05). There was no change in Lipoprotein (a) levels. Conclusion: Pentraxin-3 was a more specific inflammatory vascular marker than C-reactive protein, and the best inflammatory marker associated with hemodialysis. Homocysteine, procalcitonin and the other small proteins could be released and removed during hemodialysis session. Further studies are needed to understand the behavior and significance of these markers after successive hemodialysis.

We hypothesize that, with elevated cerebral spinal fluid (CSF) pressure, cerebral micro-vascular obstruction and congestion may occur despite (subdural) large-vein pressures being normal. Smaller veins emptying into these larger, dura-enveloped veins are not immune to the compressive effects of elevated CSF pressure and a “Starling Resistor” mechanism might explain why elevated CSF pressures collapse these smaller veins. This small cerebral venous starling resistor compression mechanism may be the final common pathway for many patients suffering from increased CSF pressures and might also be an important contributor to impaired focal venous drainage presenting as a headache with normal venous sinus pressures.

Purpose: This was a prospective study conducted at Benha University hospital and National Heart Institute on one hundred patients undwent coronary artery bypass grafting (CABG) to evaluate the effect of CABG on the right ventricular (RV) function using speckle tracking echocardiography (STE). Methods: All cases were subjected to detailed medical history, full physical examination, 12 leads electrocardiogram (ECG), routine laboratory tests including (complete blood picture, liver functions, renal functions and lipid profile) and echocardiography either conventional echocardiography or STE, all parameters obtained before and within 2 weeks after surgery. Results: By conventional echocardiography there was statistically significant decrease in peak right ventricle systolic velociy (RVS) from (12.76 ± 1.72) to (7.33 ± 1.71) and tricuspid annular plane systolic excursion (TAPSE) from (22.8 ± 3.99) to (13.77 ± 4.63) among the studied patients after CABG. While there was significant increase in right ventricle fractional area change (RVFAC) from (44.69 ± 3.25) to (49.01 ± 3.36). On the other hand, there was non-significant change in right ventricle end diastolic diameter (RVEDD) at mid-cavity from (26.37 ± 2.72) to (26.53 ± 2.72) and basal segment from (36.05 ± 2.98) to (36.29 ± 3.04), right ventricle stroke volume (RVSV) from (65.44 ± 7.02) to (65.85 ± 6.86) and right myocardial performance index (RMPI) from (0.491 ± 0.088) to (0.498 ± 0.086). By STE There was statistically significant decrease in right ventricle global longitudinal strain (RVGLS) from (-20.63 to -14.1) after CABG. There was statistically significant decrease in right ventricle free wall longitudinal strain [apical decreased from (-23.73 to -13.7), mid-cavity decreased from (-25.76 to -11.53), basal decreased from (-20.39 to -10.13) and lateral wall declined from (-23.01 to -9.13)]. There was statistically significant decrease in interventricular septum longitudinal strain [apical decreased from (-19.77 to -10.06), mid-cavity decreased from (-17.81 to -10.87) and basal decreased from (-15.89 to -11.13)]. There was statistically significant increase in RV circumferential strain of lateral free wall from (-12.04 to -16.21), while there was non-significant change in RV circumferential strain of septum from (-19.77 ± 4.86) to (-20.37 ± 5.14). Conclusion: Distorted RV geometry after CABG can lead to altered deformation parameters, in other words longitudinal functional parameters may underestimate RV function and the decrease in RVGLS was compensated by increase in circumferential strain of lateral free wall of RV without change in RVSV or RMPI. Therefor changes in deformation parameters should always be interpreted in relation to change in geometry.

A 56-year-old man was admitted to our hospital because of sudden onset of right-sided thoracic pain. The ECG showed inferior ST segment elevations. He has been treated with aspirin, clopidogrel, unfractionated heparin and tenecteplase, and his symptoms resolved after 30 minutes. About half an hour later, the patient developed again left-sided thoracic pain and the signs of an anterior myocardial ST-segment elevation infarction. 90 minutes after receiving the initial medications, the performed coronary angiography revealed a long dissection of a large ramus circumflexus. Furthermore, the left anterior descending coronary artery was occluded at about the mid-level. The left ventriculography showed a reduced ventricular function and a Stanford type A aortic dissection. Immediate patient transfer for emergency surgical intervention was arranged. However, ventricular fibrillation occurred during transport and he required endotracheal intubation and prolonged cardiopulmonary resuscitation. Unfortunately, he died during further transport. In a patient with massive thoracic pain of initially uncommon localization in combination with fluctuation of ST-segment elevations, aortic dissection should be seriously taken into the differential diagnosis as well as into therapeutic management decisions (in particular antiplatelet and thrombolytic therapy).