Myocardial mechanical and QTc dispersion for the detection of significant coronary artery disease.

AIMS: Ischaemic but viable myocardium may exhibit prolongation of contraction and QT interval duration, but it is largely unknown whether non-invasive assessment of regional heterogeneities of myocardial deformation and QT interval duration could identify patients with significant coronary artery disease (CAD). METHODS AND RESULTS: We retrospectively studied 205 patients with suspected CAD who underwent coronary angiography. QTc dispersion was assessed from a 12-lead electrocardiogram (ECG) as the difference between the longest and shortest QTc intervals. Contraction duration was assessed as time from the ECG R-(Q-)wave to peak longitudinal strain in each of 18 left ventricular segments. Mechanical dispersion was defined as either the standard deviation of 18 time intervals (dispersionSD18) or as the difference between the longest and shortest time intervals (dispersiondelta). Longitudinal strain was measured by speckle tracking echocardiography. Mean contraction duration was longer in patients with significant CAD compared with control subjects (428 ± 51 vs. 410 ± 40 ms; P = 0.032), and it was correlated to QTc interval duration (r = 0.47; P < 0.001). In contrast to QTc interval duration and dispersion, both parameters of mechanical dispersion were independently associated with CAD (P < 0.001) and had incremental value over traditional risk factors, wall motion abnormalities, and global longitudinal strain (GLS) for the detection of significant CAD. CONCLUSION: The QTc interval and myocardial contraction duration are related to the presence of significant CAD in patients without a history of previous myocardial infarction. Myocardial mechanical dispersion has an incremental value to GLS for identifying patients with significant CAD.

Interrelatedness between C-reactive protein and oxidized low-density lipoprotein.

C-reactive protein (CRP) is a marker of inflammation. Atherosclerosis is now recognized as inflammatory disease, and it seems that CRP directly contributes to atherogenesis. Oxidation of low-density lipoprotein (LDL) molecule increases the uptake of lipid products by macrophages leading to cholesterol accumulation and subsequent foam cell formation. The elevated levels of high sensitivity CRP (hsCRP) and oxidized LDL (OxLDL) in the blood were found to be associated with cardiovascular diseases (CVD). In this review, we highlighted the evidence that CRP and OxLDL are involved in interrelated (patho) physiological pathways. The findings on association between hsCRP and OxLDL in the clinical setting will be also summarized.

Visual assessment vs. strain imaging for the detection of critical stenosis of the left anterior descending coronary artery in patients without a history of myocardial infarction.

AIMS: We sought to determine the prevalence of overt and subclinical LV dysfunction in patients with critical left anterior descending coronary artery (LAD) stenosis but without a history of myocardial infarction and to compare diagnostic value of routine echocardiographic parameters with myocardial strain analysis for detection of critical LAD stenosis. METHODS AND RESULTS: We retrospectively studied 269 patients with suspected coronary artery disease (CAD)-209 consecutive patients with critical LAD stenosis and 60 consecutive patients with atypical chest pain and without CAD. Conventional visual assessment of LV asynergy in the LAD territory was compared with global, regional, and segmental peak systolic longitudinal strain (PSLS) parameters derived by two-dimensional speckle tracking echocardiography (2D STE). Wall motion abnormalities in the LAD territory were found in 41% of patients with critical LAD stenosis, whereas, depending on the cut-off value, global longitudinal strain (GLS) was impaired in 42-69% of patients. GLS with an area under the receiver operating characteristic curve (AUC) of 0.85 showed better discriminative power for detecting critical LAD stenosis than conventional wall motion score index (AUC 0.73, P < 0.05, for the difference between the AUCs). PSLS values were significantly lower in basal and midventricular segments supplied by critically narrowed LAD, particularly if they also appeared dysfunctional on visual assessment. CONCLUSIONS: Detection of subclinical LV dysfunction by 2D STE might improve identification of patients with critical LAD stenosis, although visually apparent regional LV dysfunction in the LAD territory is not uncommon finding in this subset of patients.

Spontaneous coronary artery dissection- rare but challenging.

INTRODUCTION: Spontaneous coronary artery dissection (SCAD) is a rare cause of the acute coronary syndrome. It occurs mostly in patients without atherosclerotic coronary artery disease, carrying fairly high early mortality rate. The treatment of choice (interventional, surgical, or medical) for this serious condition is not well-defined. CASE REPORT: A 41-year old woman was admitted to our hospital after the initial, unsuccessful thrombolytic treatment for anterior myocardial infarction administered in a local hospital without cardiac catheterization laboratory. Immediate coronary angiography showed spontaneous coronary dissection of the left main and left anterior descending coronary artery. Follow-up coronary angiography performed 5 days after, showed extension of the dissection into the circumflex artery. Because of preserved coronary blood flow (thrombolysis in myocardial infarction - TIMI II-III), and the absence of angina and heart failure symptoms, the patient was treated medicaly with dual antiplatelet therapy, a low molecular weight heparin, a beta-blocker, an angiotensin-converting enzyme (ACE) inhibitor and a statin. The patient was discharged after 12 days. On follow-up visits after 6 months and 2 years, the patient was asymptomatic, and coronary angiography showed the persistence of dissection with preserved coronary blood flow. CONCLUSION: Immediate coronary angiography is necessary to assess the coronary anatomy and extent of SCAD. In patients free of angina or heart failure symptoms, with preserved coronary artery blood flow, medical therapy is a viable option. Further evidence is needed to clarify optimal treatment strategy for this rare cause of acute coronary syndrome.

Two-dimensional speckle tracking-derived strain to distinguish acute coronary syndrome from a marked early repolarization in a patient with chest pain: a fancy gadget or a useful tool?

BACKGROUND: With a potential of detecting subtle myocardial injury, two-dimensional (2D) speckle tracking-derived strain could help to distinguish between ischemic and nonischemic ST-segment elevation. Little is known if limitations of strain imaging could prevent its applicability in acute cardiac care settings. CASE PRESENTATION: We present a 56-year-old male with persistent ST-segment elevation in the inferolateral leads and suspected hypokinesia of the inferior wall. Semiautomated 2D speckle tracking strain analysis showed normal longitudinal peak systolic strain (LPSS) in all segments of the inferior wall, ruling out wall-motion abnormalities in this region. Stationary reverberations and spuriously low values of LPSS in the posterolateral wall required operator's expertise to distinguish pathological myocardial deformation from artifacts. Additional workup revealed that early repolarization pattern was mistaken for the inferior wall acute myocardial infarction in our patient. CONCLUSIONS: Semiautomated quantification of regional left ventricular function by 2D speckle tracking echocardiography could facilitate decision making even in the emergency settings. Due to intrinsic limitations of this novel method, its actual clinical value in acute cardiac care settings may depend on the expertise of the operator and is yet to be determined.

Establishing the diagnosis of inverted stress cardiomyopathy in a patient with cardiac arrest during general anesthesia: a potential role of myocardial strain?

In cardiac arrest survivors, postresuscitation myocardial stunning usually presents as either global left ventricular dysfunction or regional dyssynergy including the various forms of stress cardiomyopathy, in which rare variants may be difficult to diagnose. We present a patient with cardiac arrest during general anesthesia, in whom speckle tracking-derived myocardial strain helped to distinguish between the inverted variant of stress cardiomyopathy and global postresuscitation myocardial stunning.

Simvastatin and amlodipine induced thrombocytopenia in the same patient: double trouble and a literature review.

WHAT IS KNOWN AND OBJECTIVE: Drug-induced thrombocytopenia (DITP) may be a fatal adverse reaction to many drugs. It is often misdiagnosed as primary immune thrombocytopenia (ITP), and thus diagnosis can be delayed and patients can be treated inappropriately. Amlodipine a calcium-channel blocker, and simvastatin, a statin, have very rarely been implicated in DITP. We report on an investigation of the causal relationship of amlodipine and simvastatin with thrombocytopenia occurring in the same patient, and review the literature. CASE SUMMARY: We present the case of a 78-year-old female hypertensive diabetic patient with three successive DITPs. The first attack of acute severe thrombocytopenia occurred after a 2-week course of amlodipine, and was initially misdiagnosed as ITP. Her platelet count normalized after the amlodipine was discontinued. The second attack followed her restarting simvastatin 3 weeks later. She had stopped it 2 months earlier having previously taken it for over 5 years. Again, she recovered once the simvastatin was discontinued. The third DITP attack occurred when she accidently took a single dose of amlodipine 9 months later. WHAT IS NEW AND CONCLUSION: We provide clear evidence of a causal association of amlodipine with thrombocytopenia, and probable evidence of a causal association of simvastatin with thrombocytopenia. This is the first reported case of DITPs occurring with two of the most widely prescribed drugs in the same patient. Many hypertensive patients need to take multiple drugs in order to achieve their treatment goals and this increases their risk of drug-induced adverse reactions and makes identification of the causal drug (or drugs) extremely difficult.

The absence of the ST-segment elevation in acute coronary artery thrombosis: what does not fit, the patient or the explanation?

In a few patients with acute proximal thrombotic occlusion of the left anterior descending coronary artery (LAD), tall ischemic T waves never evolve into ST-segment elevation. This was recently inaccurately reported as a "novel sign" of proximal LAD occlusion. It has been speculated that the absence of ST-segment elevation could be attributed to the large area of transmural ischemia, the anatomic variant of Purkinje fibers, or to lack of activation of sarcolemal adenosine triphosphate-potassium channels. This electrocardiographic picture was recently explained by changes in the subendocardial but not in the epicardial action potential, suggesting subendocardial ischemia as the underlying mechanism. We present a patient with thrombotic lesion of proximal LAD, static precordial ST-segment depression, and tall T waves who underwent primary percutaneous intervention and stent placement. Surprisingly, total thrombotic stent occlusion on the following day was associated with ST-segment elevation in precordial leads, indeed supporting the concept of the regional subendocardial ischemia that was first described more than a decade ago.

[Pseudopacemaker syndrome and marked first-degree atrioventricular block: case report].

INTRODUCTION: Pacemaker syndrome consists of the symptoms and signs present in the single chamber (VVI) pacemaker patient with electrode placed in the right ventricular apex. It is caused by inadequate timing of atrial and ventricular contractions. Pacemaker syndrome without a pacemaker (or pseudopacemaker syndrome) refers to occurrence of symptoms in the presence of marked first-degree atrioventricular (AV) block, when P wave is too close to the preceding QRS complex producing the same haemodynamic disturbance as artificial pacemaker cardiac stimulation with retrograde VA conduction. CASE OUTLINE: We present the patient with acute inferior myocardial infarction due to late bare metal stent thrombosis, treated with primary pectutaneous coronary intervention. Hospital course was complicated by complete heart block which was treated with temporary pacing. During the stand-by mode of temporary pacing, sinus rythm with marked first-degree AV block (PQ interval 480 ms) was observed while the patients re-experienced the symptoms that were present prior to pacemaker implantation. Temporary pacing was continued for the next 24 hours when spontaneous shorteninig of PQ interval (250-270 ms) was noticed; since the patient was asymptomatic during the stand-by mode, the pacemaker electrodes were removed and the patient discharged 11 days after admission. CONCLUSION: Conduction disturbances, such as the varying degrees of AV blocks, are relatively common in acute inferior myocardial infarction. The first degree AV blok is usually asymptomatic and does not require treatment, unless when it is associated with pseudopacemaker syndrome. In that case, temporary pacing provides haemodynamic stability until conduction system recovers.

[Takotsubo cardiomyopathy: report of the first case series in Serbia and review of the literature].

INTRODUCTION: Takotsubo cardiomyopathy is a relatively novel cardiac syndrome that is characterized by transient left ventricular asynergy involving apical and mid-ventricular segments. EPIDEMIOLOGY AND PATHOPHYSIOLOGY: It occurs predominantly in elderly women in the absence of obstructive coronary artery disease and is usually associated with severe emotional or physical stress. This syndrome is manifested with chest pain, electrocardiographic changes that mimic acute myocardial infarction, and minimal myocardial enzymatic release. Several different mechanisms have been proposed: coronary artery spasm, dynamic left ventricular outflow/ intracavitary obstruction, coronary microvascular dysfunction and direct catecholamine-mediated cardiomyocite injury. THERAPY AND PROGNOSIS: Complete recovery usually occurs after dramatic presentation, frequently complicated with acute heart failure. Therapy is empiric and directed towards supportive measures against cardiogenic shock, acute heart failure, dysrhythmias. In-hospital mortality rate is less than 1%, but long-term prognosis is still unknown. In addition to the review of the literature on takotsubo cardiomyopathy, we present the first series of patients with this syndrome detected in Clinical Hospital Center Zemun.