Cognitive Impairment in Cardiovascular Patients after Myocardial Infarction: Prospective Clinical Study.

(1) Background: Assessment of cognitive function is not routine in cardiac patients, and knowledge on the subject remains limited. The aim of this study was to assess post-myocardial infarction (MI) cognitive functioning in order to determine the frequency of cognitive impairment (CI) and to identify factors that may influence it. (2) Methods: A prospective study included 468 patients hospitalized for MI. Participants were assessed twice: during the first hospitalization and 6 months later. The Mini-Mental State Examination was used to assess the occurrence of CI. (3) Results: Cognitive dysfunction based on the MMSE was found in 37% (N-174) of patients during the first hospitalization. After 6 months, the prevalence of deficits decreased significantly to 25% (N-91) (p < 0.001). Patients with CI significantly differed from those without peri-infarction deficits in the GFR, BNP, ejection fraction and SYNTAX score, while after 6 months, significant differences were observed in LDL and HCT levels. There was a high prevalence of non-cognitive mental disorders among post-MI patients. (4) Conclusions: There is a high prevalence of CI and other non-cognitive mental disorders, such as depression, sleep disorders and a tendency to aggression, among post-MI patients. The analysis of the collected material indicates a significant impact of worse cardiac function expressed as EF and BNP, greater severity of coronary atherosclerosis expressed by SYNTAX results, and red blood cell parameters and LDL levels on the occurrence of CI in the post-MI patient population.

TAKOTSUBO SYNDROME AND CORONARY ARTERY FISTULA: CASE REPORT AND LITERATURE REVIEW.

Takotsubo syndrome (TTS) has been reported in various clinical conditions. Coronary artery fistula (CAF) is diagnosed in 0.2- 0.4% of patients undergoing coronary angiography. Pathologic communication between coronary artery (e.g., left anterior de¬scending coronary artery - LAD) and cardiac chambers (e.g., left ventricle - LV) is cameral type of CAF which particularly predis¬pose to myocardial ischemia due to a steal syndrome. Eight cases of coexistent TTS and CAF have been reported so far; in 6 of them LAD cameral fistulas drained LV, in 2 others communications between coronary arteries and pulmonary artery were found. The authors describe a case of a 75-year-old female, admitted due to chest pain and dyspnea. Her clinical picture with ST-segment elevation in ECG, moderately increased troponin I and apical ballooning in echocardiography, was more typical for TTS than for myocardial infarction; besides that, color doppler imaging was suggestive of multiple CAF to LV. Coronary angiography showed communication between all (normal) coronary arteries and LV. Throughout the conservative therapy, first, an improve¬ment and then normalization of LV function were observed after 2 and 6 days, respectively. Chest x-ray and computed tomogra¬phy revealed mediastinal tumor (eventually diagnosed as lung cancer). Cardiac magnetic resonance performed after one month did not show late gadolinium enhancement. During the course of 24 months follow-up, she was taking bisoprolol and ramipril and her cardiologic state remained stable, even during chemotherapy and radiotherapy. The authors collected the clinical data of all 9 cases with concomitant TTS and CAF. Specific TTS triggering factors/predisposing conditions were present in all patients, which has indicated that coexistence of TTS and CAF is rather coincidental.

Multimodality imaging of mitral annular disjunction.

Mitral valve prolapse (MVP) is diagnosed by auscultation and echocardiography in about 2-3% of the general population and takes rather a benign course. However, in some patients, ventricular arrhythmia and sudden cardiac death (SCD) occur, which is linked to mitral annular disjunction (MAD). MAD is defined as distinct separation of the mitral valve annulus-left atrial wall continuum and the basal region of the posterolateral left ventricular (LV) myocardium. MAD results in disturbed inferior-posterior LV wall and posteromedial papillary muscle stretch giving rise to local fibrosis presenting in cardiac magnetic resonance (CMR) as late gadolinium enhancement (LGE) and posing a substrate for malignant arrhythmia. Multidetector-row computed tomography (MDCT) in MAD patients is still rarely used. A CASE REPORT: Mitral valve prolapse (MVP) is diagnosed by auscultation and echocardiography in about 2-3% of the general population and takes rather a benign course. However, in some patients, ventricular arrhythmia and sudden cardiac death (SCD) occur, which is linked to mitral annular disjunction (MAD). MAD is defined as distinct separation of the mitral valve annulus-left atrial wall continuum and the basal region of the posterolateral left ventricular (LV) myocardium. MAD results in disturbed inferior-posterior LV wall and posteromedial papillary muscle stretch giving rise to local fibrosis presenting in cardiac magnetic resonance (CMR) as late gadolinium enhancement (LGE) and posing a substrate for malignant arrhythmia. Multidetector-row computed tomography (MDCT) in MAD patients is still rarely used.

Takotsubo syndrome after nimodipine-induced hypotension treated with norepinephrine in a female with subarachnoid hemorrhage.

The prevalence of takotsubo syndrome (TTS) in patients with subarachnoid hemorrhage (SAH) is much higher than in the general population. Clinical and experimental observations confirm secondary to brain damage catecholamine-mediated cardiac injury resulting in reversible left ventricular (LV) dysfunction. However, other triggers can also be involved in TTS development e.g. manipulations during surgical or endovascular treatment of a bleeding intracranial aneurysm, concomitant hyponatremia or infection, intubation, blood transfusion and pharmacologic treatment. Nimodipine is recommended in SAH to prevent cerebral arteries vasospasm but can cause hypotension, so vasopressors, e.g. norepinephrine (NE) are commonly used to reach target blood pressure. A CASE REPORT: The authors present a case of a 72-year-old woman with SAH in whom the disease began with a headache, syncope, decreased level of consciousness and vomiting; there were no cardiac symptoms at admission. Endovascular coiling of internal carotid artery aneurysm was performed. On day 2, she developed TTS presenting in echocardiography as apical ballooning; immediately before TTS onset, NE was started to treat nimodipine-induced hypotension. Despite severe heart failure (HF), the patient's neurological status did not deteriorate. HF symptoms remitted after a few days and LV function returned to normal after a week. Negative T waves in ECG which appeared at TTS onset disappeared after 50 days. At that moment no neurological deficits were observed. CONCLUSIONS: The authors underline that in SAH patients nimodipine administration should be cautious to avoid an excessive blood pressure decrease especially in view of further catecholamines use.

Asymptomatic cardiac and gallbladder involvement at initial presentation of Legionnaires' disease.

Extrapulmonary manifestations of Legionnaires' disease (LD) include, inter alia cardiac, brain, abdominal, joints and skin involvement. A CASE REPORT: The authors describe a case of a 41-year-old immunocompetent female admitted due to a high fever, chills and fatigue. She negated cough and chest or abdominal pain. Initial chest X-ray was normal. Among laboratory abnormalities were: elevation of C-reactive protein, procalcitonin, transaminases and creatinine, hyponatremia, low white blood cell and platelet count and a moderate proteinuria. ECG showed subtle ST elevation. Echocardiography revealed normal left ventricular (LV) contractility and near normal longitudinal strain, mild myocardial thickening, and a small pericardial effusion; additionally, in subcostal view, gallbladder wall thickening (GBWT) was found. Positive L. pneumophila urinary antigen test confirmed LD diagnosis. Control Xray and CT showed development of pleural effusion and bilateral pulmonary infiltrations. Clinical and radiologic improvement of the disease was achieved with ciprofloxacin therapy started from admission. ECG abnormalities persisted for only 5 days, GBWT resolved after 9 days, pericardial effusion disappeared after 10 days; normalization of LV thickness and an increase in longitudinal strain was found within 2 weeks. However, cardiac magnetic resonance (CMR) performed after a month revealed focal midmyocardial and linear subepicardial late gadolinium enhancement (LGE). CONCLUSIONS: The authors underline the fact that being aware of extrapulmonary LD, also silent, may allow to diagnose the disease, especially when pulmonary involvement is initially absent.

Transient left ventricular hypertrophy in a 30-year-old female with chronic emotional stress and depression treated with venlafaxine.

Transient left ventricular hypertrophy or thickening (TLVH/T) is a phenomenon rarely observed in some patients with myocarditis and stress-induced takotsubo syndrome (TTS). Initial presentation on echocardiography can mimic hypertrophic cardiomyopathy (HCM), sometimes with a decreased ejection fraction (EF). A CASE REPORT: The authors describe TLVH/T in a 30-year-old female with a history of chronic emotional stress and depression treated with venlafaxine (75 mg twice a day). She suffered from spinocerebellar ataxia (SCA) and, because of a family conflict, was living alone with a daughter who was diagnosed with maple syrup urine disease (MSUD). At admission, she presented with advanced heart failure with pulmonary congestion, moderately elevated blood pressure, ECG signs of LV hypertrophy (with negative T waves in leads: I-III, aVF, V4- 6) and with mild troponin I and high BNP elevation. Echocardiography revealed hypertrophy of the LV myocardium, systolic dysfunction and a small pericardial effusion. She denied any chest pain; there were no clinical features of infection or connective tissue disorder. Genetic nature of the patient's SCA and of her daughter's MSUD gave rise to a suspicion that she had coexistent HCM. She received therapy with ramipril, carvedilol and diuretics; venlafaxine was not discontinued. Cardiac magnetic resonance (CMR) performed a month later showed LV thickening to be a little smaller, absence of late gadolinium enhancement and an improvement of EF; T2-weighted images were not studied. Unexpectedly, after several months, LV hypertrophy disappeared in subsequent ECG, echocardiography and CMR; simultaneously, EF as well as regional and longitudinal strain returned to normal values.

[Rivaroxaban-resistant right ventricular thrombus, successfully treated with vitamin K antagonist in a patient with dilated cardiomyopathy]. / Oporna na rywaroksaban skrzeplina w prawej komorze, skutecznie leczona antagonista witaminy K u chorego z kardiomiopatia rozstrzeniowa.

Rivaroxaban, a selective inhibitor of active factor X belongs to the group of direct-acting oral anticoagulants (DOAC), more and more often replacing vitamin K antagonists (VKA) in venous thromboembolic disease and nonvalvular atrial fibrillation. Attempts are also being made to use DOAC to treat locally formed intracardiac thrombi, mainly in the left atrium and its appendage, in atrial fibrillation and in heart failure. Rarely diagnosed local right ventricular thrombus (RVT) may be a complication of dilated cardiomyopathy (DCM). CASE REPORT: The authors present a case of a 40-year-old male with DCM and RVT located in the apex, which was imaged in echocardiography, magnetic resonance and multislice computed tomography. During treatment with rivaroksaban (2x15 mg: 4 weeks; 1x20 mg: 4 months) diminishing of RVT was not observed. After 2 months of VKA use complete resolution of RVT was noted. The case presented is probably the first described RVT treated with rivaroxaban. The authors conclude that in some cases, anticoagulation with VKA may be more effective than DOAC in intracardiac thrombi therapy, especially when it is meticulously monitored. Overlapping effect on RVT due to anticoagulants use with a different mechanism of action cannot be excluded.

Evaluation of plasma PCSK9 concentrations, transcript of LDL receptor, as well as the total number of monocyte LDL receptors in acute coronary syndrome patients.

BACKGROUND: Before our study, there were no data concerning complex evaluation of: plasma PCSK9 concentrations, transcript LDL receptor (LDLR), as well as the total amount of monocytes' LDLR in acute coronary syndrome (ACS) patients. PCSK9 levels in a few cohort studies were found to correlate with the number of white blood cells (WBC) or platelets (PLT). The study aims to evaluate PCSK9-LDLR concentrations, as well as to find any association between PCSK9 and WBC or PLT. METHODS: The study group included 95 consecutive patients with acute myocardial infarction, in whom angiography/angioplasty of the culprit vessel was performed. The control group consisted of 10 healthy young volunteers. Thirty patients from the studied group were qualified for further percutaneous revascularization after 3 months. Laboratory tests were performed using commercially available kits. LDLR expression on monocyte surface was measured by flow cytometry, but the mRNA level for LDLR was established by real time polymerase chain reaction. The PCSK9 plasma concentration was measured by ELISA kits. RESULTS: Higher concentration of PCSK9 and amount of LDLR on monocytes surface were observed in patients with ACS compared with healthy young volunteers (number of LDLRs on monocytes [reaction units] 10.8 ± 9.6 vs. 41.8 ± 11.8, p < 0.001, PCSK9 [ng/mL] 295.4 ± 76.4 vs. 213 ± 63.2, p < 0.001). A similar relationship was observed after application of 3-month intensive lipid-lowering therapy in patients with ACS (n = 30, PCSK9 [ng/mL] 281.1 ± 59.5 vs. 358.5 ± 74.7, p < 0.001, LDLR transcript [reaction units] 0.6 ± 0.32 vs. 1.87 ± 0.24, p < 0.001, number of LDLRs on monocytes [reaction units] 5.9 ± 3.1 vs. 22.3 ± 3.8, p < 0.001). There were no significant differences in levels of PCSK9, LDLR between patients with ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI). There was no relation of the PCSK9 with WBC as well as with PLT. CONCLUSIONS: We observed significantly higher concentration of PCSK9, and significantly higher levels of mRNA LDLR transcript in patients with ACS compared with healthy young volunteers. A similar pattern was observed after 3 months of intensive statin therapy among patients with ACS. There were no differences in these parameters between patients with STEMI vs. NSTEMI. The results of the study require confirmation in a larger population of patients.

[Myopericarditis in a 23-year-old male with herpes zoster]. / Zapalenie miesnia serca i osierdzia u 23-letniego mezczyzny z pólpascem.

The varicella zoster virus (VZV) belongs to cardiotropic viruses, although the frequency of cardiac complications during VZV infection is low. Diagnosis of myocarditis or myopericarditis is rare during varicella - primary infection of VZV and sporadic in zoster - reactivation of latent VZV. Only few such cases have been described. The authors present a case of a 23-year-old male in whom clinical symptoms of myopericarditis developed a week after diagnosis of zoster that was localized in the left-upper part of the thorax. Retrosternal chest pain and fever were accompanied by ECG mimicking acute myocardial infarction. A dynamic pattern of troponin I release and slow normalization of ECG were observed. Serial echocardiography showed normal left ventricular function, transient changes in echogenicity of the interventricular septum and small pericardial effusion. In magnetic resonance imaging subepicardial and intramyocardial areas of late gadolinium enhancement were found. He was treated with intravenous acyclovir. No late sequels of the disease were observed.