Primary Left Atrial Angiosarcoma Presenting as Acute Coronary Syndrome.

Primary cardiac neoplasms are extremely rare and often overlooked as differential diagnosis. Angiosarcomas are the most common primary malignant neoplasms of the heart often with nonspecific symptoms. We present a 43-year-old woman admitted to our hospital with chest pain and inferoposterolateral myocardial infarction. Coronary angiography indicated the distal occlusion of the left circumflex artery. Transthoracic and transoesophagic echocardiography revealed a mass in the left atrium with probable myocardial infiltration and vascularisation. The mass in the left atrium was removed by surgical resection, and histopathology confirmed angiosarcoma. We emphasize the pivotal role of transthoracic and transoesophageal echocardiography in evaluating even rare differential diagnosis of acute coronary syndrome as cardiac neoplasms.

Longitudinal analysis of chest Q-SPECT/CT in patients with severe COVID-19.

INTRODUCTION: Patients with COVID-19 have an increased risk for microvascular lung thrombosis. In order to evaluate the type and prevalence of perfusion defects, we performed a longitudinal analysis of combined perfusion single-photon emission and low-dose computed tomography (Q-SPECT/CT scan) in patients with COVID-19 pneumonia. METHODS: Consecutive patients with severe COVID-19 (B.1.1.7 variant SARS-CoV-2) and respiratory insufficiency underwent chest Q-SPECT/CT during hospitalization, and 3 months after discharge. At follow-up (FU), Q-SPECT/CT were analyzed and compared with pulmonary function tests (PFT), blood analysis (CRP, D-dimers, ferritin), modified Medical Research Council (mMRC) dyspnea scale, and high-resolution CT scans (HRCT). Patients with one or more segmental perfusion defects outside the area of inflammation (PDOI) were treated with anticoagulation until FU. RESULTS: At baseline, PDOI were found in 50 of 105 patients (47.6 %). At FU, Q-SPECT/CT scans had improved significantly (p < 0.001) and PDOI were recorded in 14 of 77 (18.2 %) patients. There was a significant correlation between mMRC score and the number of segmental perfusion defects (r = 0.511, p < 0.001), and a weaker correlation with DLCO (r = -0.333, p = 0.002) and KCO (r = -0.373, p = 0.001) at FU. Neither corticosteroid therapy nor HRCT results showed an influence on Q-SPECT/CT changes (p = 0.94, p = 0.74). CRP, D-Dimers and ferritin improved but did not show any association with the FU Q-SPECT/CT results (p = 0.08). CONCLUSION: Segmental mismatched perfusion defects are common in severe COVID-19 and are correlated with the degree of dyspnea. Longitudinal analyses of Q-SPECT/CT scans in severe COVID-19 may help understand possible mechanisms of long COVID and prolonged dyspnea.

The prevalence of smoking among Croatian hospitalized coronary heart disease patients.

The aim of this paper was to investigate the prevalence of smoking using selected anthropometric variables in a sample of hospitalized coronary heart disease (CHD) patients in Croatia (N = 1,298). A total of 444 subjects (34.6%) were non-smokers, 548 (42.6%) were smokers and 293 (22.8%) were ex-smokers. Men, on average, smoked more cigarettes per day than women (22.62 vs. 19.84 cigarettes, p < 0.001) and they also had bigger index "pack-years" than women (36.96 vs. 33.91, p = 0.024). Men were more often smokers and ex-smokers than women (47.4% vs. 30.8% for smokers and 25.0% vs. 22.8% for ex-smokers, p < 0.001). In this study a high prevalence of smoking was found among CHD patients in Croatia. Unless it is decreased, it can be expected that CHD patients in Croatia will continue to experience adverse effects more often than other CHD patients in the rest of Europe.

A biallelic loss-of-function variant in MYZAP is associated with a recessive form of severe dilated cardiomyopathy.

PURPOSE: Dilated cardiomyopathy (DCM) is a primary disorder of the cardiac muscle, characterised by dilatation of the left ventricle and contractile dysfunction. About 50% of DCM cases can be attributed to monogenic causes, whereas the aetiology in the remaining patients remains unexplained. METHODS: We report a family with two brothers affected by severe DCM with onset in the adolescent period. Using exome sequencing, we identified a homozygous premature termination variant in the MYZAP gene in both affected sibs. MYZAP encodes for myocardial zonula adherens protein - a conserved cardiac protein in the intercalated disc structure of cardiomyocytes. RESULTS: The effect of the variant was demonstrated by light and electron microscopy of the heart muscle and immunohistochemical and Western blot analysis of MYZAP protein in the heart tissue of the proband. Functional characterization using patient-derived induced pluripotent stem cell cardiomyocytes revealed significantly lower force and longer time to peak contraction and relaxation consistent with severe contractile dysfunction. CONCLUSION: We provide independent support for the role of biallelic loss-of-function MYZAP variants in dilated cardiomyopathy. This report extends the spectrum of cardiac disease associated with dysfunction of cardiac intercalated disc junction and sheds light on the mechanisms leading to DCM.

Stable Gastric Pentadecapeptide BPC 157 as Useful Cytoprotective Peptide Therapy in the Heart Disturbances, Myocardial Infarction, Heart Failure, Pulmonary Hypertension, Arrhythmias, and Thrombosis Presentation.

In heart disturbances, stable gastric pentadecapeptide BPC 157 especial therapy effects combine the therapy of myocardial infarction, heart failure, pulmonary hypertension arrhythmias, and thrombosis prevention and reversal. The shared therapy effect occurred as part of its even larger cytoprotection (cardioprotection) therapy effect (direct epithelial cell protection; direct endothelium cell protection) that BPC 157 exerts as a novel cytoprotection mediator, which is native and stable in human gastric juice, as well as easily applicable. Accordingly, there is interaction with many molecular pathways, combining maintained endothelium function and maintained thrombocytes function, which counteracted thrombocytopenia in rats that underwent major vessel occlusion and deep vein thrombosis and counteracted thrombosis in all vascular studies; the coagulation pathways were not affected. These appeared as having modulatory effects on NO-system (NO-release, NOS-inhibition, NO-over-stimulation all affected), controlling vasomotor tone and the activation of the Src-Caveolin-1-eNOS pathway and modulatory effects on the prostaglandins system (BPC 157 counteracted NSAIDs toxicity, counteracted bleeding, thrombocytopenia, and in particular, leaky gut syndrome). As an essential novelty noted in the vascular studies, there was the activation of the collateral pathways. This might be the upgrading of the minor vessel to take over the function of the disabled major vessel, competing with and counteracting the Virchow triad circumstances devastatingly present, making possible the recruitment of collateral blood vessels, compensating vessel occlusion and reestablishing the blood flow or bypassing the occluded or ruptured vessel. As a part of the counteraction of the severe vessel and multiorgan failure syndrome, counteracted were the brain, lung, liver, kidney, gastrointestinal lesions, and in particular, the counteraction of the heart arrhythmias and infarction.

Stable Gastric Pentadecapeptide BPC 157 May Counteract Myocardial Infarction Induced by Isoprenaline in Rats.

We revealed that the stable gastric pentadecapeptide BPC 157, a useful peptide therapy against isoprenaline myocardial infarction, as well as against isoprenaline myocardial reinfarction, may follow the counteraction of the recently described occlusion-like syndrome, induced peripherally and centrally, which was described for the first time in isoprenaline-treated rats. BPC 157 (10 ng/kg, 10 µg/kg i.p.), L-NAME (5 mg/kg i.p.), and L-arginine (200 mg/kg i.p.) were given alone or together at (i) 30 min before or, alternatively, (ii) at 5 min after isoprenaline (75 or 150 mg/kg s.c.). At 30 min after isoprenaline 75 mg/kg s.c., we noted an early multiorgan failure (brain, heart, lung, liver, kidney and gastrointestinal lesions), thrombosis, intracranial (superior sagittal sinus) hypertension, portal and caval hypertension, and aortal hypotension, in its full presentation (or attenuated by BPC 157 therapy (given at 5 min after isoprenaline) via activation of the azygos vein). Further, we studied isoprenaline (75 or 150 mg/kg s.c.) myocardial infarction (1 challenge) and reinfarction (isoprenaline at 0 h and 24 h, 2 challenges) in rats (assessed at the end of the subsequent 24 h period). BPC 157 reduced levels of all necrosis markers, CK, CK-MB, LDH, and cTnT, and attenuated gross (no visible infarcted area) and histological damage, ECG (no ST-T ischemic changes), and echocardiography (preservation of systolic left ventricular function) damage induced by isoprenaline. Its effect was associated with a significant decrease in oxidative stress parameters and likely maintained NO system function, providing that BPC 157 interacted with eNOS and COX2 gene expression in a particular way and counteracted the noxious effect of the NOS-blocker, L-NAME.

[European guidelines on the diagnosis and management of pulmonary embolism]. / Smjernice Europskoga kardioloskog drustva za dijagnosticiranje i lijecenje plucne embolije.

We report on the 2008 update of Guidelines on the diagnosis and management of acute pulmonary embolism (PE) of the European Society of Cardiology that have been endorsed and recommended by the Croatian Cardiac Society. The guidelines focus on currently available and validated methods of diagnosis, prognostic assessment (prediction of outcome and death risk), treatment of pulmonary embolism and management in specific settings including pregnancy, malignancy, non-thrombotic PE, right heart thrombi, heparin-induced thrombocytopenia, chronic thromboembolic pulmonary hypertension. The novelty of these guidelines is the stratification of PE into high-risk, low-risk and intermediate-risk of PE-related early death, which has important consequences for treatment, rather than the use of misleading terms such as zmassive', zsubmassive' and znon-massive' pulmonary embolism. The anticoagulants remain the mainstay of therapy, with thrombolytic therapy being an therapeutic option in patients with high-risk PE presenting with cardiogenic shock and/or persistent arterial hypotension.

Late-onset cytomegalovirus pneumonitis successfully treated by cytomegalovirus immunoglobulin in heart transplant patient with renal failure.

Cytomegalovirus infection is one of the most serious pathogens affecting solid organ transplant recipients. Cytomegalovirus has been identified as a risk factor for graft rejection, cardiac allograft vasculopathy and is associated with increased morbidity and mortality. Viral clearance is not achieved in all patients despite standard antiviral therapy; therefore, there is great interest in prevention and treatment strategies, as use of specific cytomegalovirus immunoglobulin, to avoid progression to organ involvement. Dose regimen of specific cytomegalovirus immunoglobulin is not well studied, especially in cytomegalovirus disease. We present the case of late onset of tissue invasive disease, pneumonitis, in young female patient after heart transplantation with acute renal failure, successfully treated with frequent intermittent cytomegalovirus immunoglobulin followed by renal dosed ganciclovir.

Stable Gastric Pentadecapeptide BPC 157 Therapy for Monocrotaline-Induced Pulmonary Hypertension in Rats Leads to Prevention and Reversal.

Background. Monocrotaline selectively injures the lung's vascular endothelium and induces pulmonary arterial hypertension. The stable gastric pentadecapeptide BPC 157 acts as a prototype cytoprotective agent that maintains endothelium, and its application may be a novel therapy. Besides, BPC 157 prevents and reverses thrombosis formation, maintains platelet function, alleviates peripheral vascular occlusion disturbances, and has anti-arrhythmic and anti-inflammatory effects. Monocrotaline-induced pulmonary arterial hypertension in rats (wall thickness, total vessel area, heart frequency, QRS axis deviation, QT interval prolongation, increase in right ventricle systolic pressure and bodyweight loss) can be counteracted with early or delayed BPC 157 therapy. Methods and Results. After monocrotaline (80 mg/kg subcutaneously), BPC 157 (10 µg/kg or 10 ng/kg, days 1-14 or days 1-30 (early regimens), or days 14-30 (delayed regimen)) was given once daily intraperitoneally (last application 24 h before sacrifice) or continuously in drinking water until sacrifice (day 14 or 30). Without therapy, the outcome was the full monocrotaline syndrome, marked by right-side heart hypertrophy and massive thickening of the precapillary artery's smooth muscle layer, clinical deterioration, and sometimes death due to pulmonary hypertension and right-heart failure during the 4th week after monocrotaline injection. With all BPC 157 regimens, monocrotaline-induced pulmonary arterial hypertension (including all disturbed parameters) was counteracted, and consistent beneficial effects were documented during the whole course of the disease. Pulmonary hypertension was not even developed (early regimens) as quickly as the advanced pulmonary hypertension was rapidly attenuated and then completely eliminated (delayed regimen). Conclusions. Thus, pentadecapeptide BPC 157 prevents and counteracts monocrotaline-induced pulmonary arterial hypertension and cor pulmonale in rats.

[Role of echocardiography in acute coronary syndrome]. / Uloga ehokardiografije u akutnom koronarnom sindromu.

This article reviews the diagnostic and clinical role of echocardiography in acute coronary syndrome (ACS). The diagnosis of ACS is based on the medical history data, ECG and cardiac enzymes. Echocardiography is an accurate, inexpensive, rapid and noninvasive test, which has a diagnostic and prognostic value and detects complications in ACS. Echocardiography can evaluate damaged myocardium and myocardium which is not involved with acute ischemia, and therefore it is recommended for establishing diagnosis in patients with chest pain and clinical evidence of structural heart damage or suspected aortic dissection, for evaluation of chest pain in patients with suspected acute myocardial ischemia with unresponsive hemodynamic instability or when other methods are undiagnostic. By localizing and quantifying segmental wall motion abnormalities, echocardiography can identify the location and extent of the ischemia. It is also the mainstay of diagnosis and evaluation of mechanical complications of myocardial infarction that include ischemic mitral and tricuspid regurgitation, ventricular and papillary muscle rupture, LV thrombi, left ventricular aneurysms and pseudoaneurysms. Echocardiography is also used for risk stratification and prognosis after myocardial infarction by assessing systolic and diastolic left ventricular function. New echocardiographic methods such as stress echocardiography and myocardial contrast echocardiography have emerged and contribute to an accurate diagnosis of ACS and better evaluation of reperfusion therapy. In emergency room and coronary care units, echocardiography as a noninvasive and inexpensive method in comparison with other established methods has significant utility in the diagnosis and management of ACS patients.

[Varicella zoster myopericarditis in an immunocompetent adult]. / Mioperikarditis izazvan virusom varicella-zoster u imunokompetentnog odraslog bolesnika.

More than 20 viruses have been reported to cause myopericarditis, a rare but potentially dangerous complication. To our best knowledge only a few dozen cases of myopericarditis caused by varicella zoster virus have been reported, most frequently in children, seldom in immunocompetent adults. We report on a case of a myopericarditis caused by varicella zoster virus in a previously healthy young man, with a typical development and a fast and complete recovery. A 27-years-old male was admitted to our hospital with chest pain and signs of acute cardiac injury. He had no medical history of serious previous illnesses. Four weeks earlier, the patient was in contact with a child having chickenpox. Two days prior to admission patient became suddenly febrile up to 40 degrees C along with dry cough, and the following day intense chest pain set in. At the admission we found in the patient diffuse vesiculous exanthema on the whole body and capillitium. Heart beat was rhythmical with no audible murmurs or pericardial friction rub, 100 beats per minute, blood pressure RR 130/90 mm Hg, body temperature 37.4 degrees C, and ST segment elevation in lateral leads along with elevated cardiac markers were found. All parameters of complete blood count were within normal range. Chest X-ray showed somewhat enlarged heart with incipient signs of cardiac decompensation. Echocardiogram was normal, apart from a mild dyskinesis of the apical third of intraventricular septum, with ejection fraction slightly reduced to 50% and no valvular defect. Clinical diagnosis of acute infection with varicella zoster virus was confirmed serologically by a positive ELISA test. Patient received conservative therapy (isosorbide mononitrate, low molecular weight heparin, acetylsalicylic acid and bisoprolol), while he remained hemodinamically, and apart from one non sustained ventricular tachycardia immediately after admission, also rhythmically stable. During his stay in hospital we observed the typical evolution and regression of rash while the levels of cardiac markers normalised, with patient becoming afebrile the third day. Before dismission a control echocardiograph showed improvement of contractile function, ejection fraction improved to 65%, but also signs of mild pericarditis were recorded. Since the patient had no discomfort and was in a very good shape, he was dismissed from hospital with ibuprofen 400 mg twice a day as therapy. Two months later, the patient was readmitted for control. In the mean time he had no discomfort, all laboratory and the physical examination findings were normal, as well as the ECG. Echocardiogram showed normal contractility, systolic and diastolic function. Cardiac stress testing and coronary angiography both ruled out a coronary heart disease. Diagnosis of myocarditis in this case was made based on echocardiogram, anamnestic data and on the typical clinical presentation of an acute varicella zoster virus infection, and was serologically confirmed by ELISA test. Therapy with NSAID was started immediately and because of favorable development of the disease we did not perform myocardial biopsy. During second hospitalization an eventual coronary heart disease was ruled out by coronary angiography. Due to its rarity there are no guidelines regarding therapy of varicella myocarditis, but there is a consensus that these patients should receive intensive care unit. The basis of the therapy are certainly the NSAIDs, but also a combination of acyclovir and hyperimmunoglobulins has been reported which in this mild case was not necessary. With this report we want to point out that varicella zoster virus can cause myopericarditis in immunocompetent adults, which must be taken into consideration in differential diagnosis, and that an early diagnosis and adequate therapy can help achieve a fast and complete recovery.

[Features and pathophysiology of acute coronary syndrome]. / Oblici i patofiziologija akutnog koronarnog sindroma.

Coronary heart disease (CHD) is the leading cause of death in developed countries, and it also has fastest growing death rates in developing countries. Patients with acute coronary syndromes (ACS) are divided into two groups - those with and those without ST segment elevation. ACS without ST segment elevation also includes unstable angina pectoris (UA) any non-ST elevation myocardial infarction (NSTEMI). It is important to note that UA is defined as ischemic chest pain at rest without a rise in serum cardiac biomarkers, while the establishment of NSTEMI diagnosis requires a rise in serum cardiac biomarkers. ACS with ST segment elevation is STEMI, and it includes both ST segment elevation and a rise in serum cardiac biomarkers. Connection of UA, NSTEMI and STEMI is based on the fact that these are closely connected conditions with similar pathogenesis and clinical presentation, but they do differ by the level of severity. The main difference lies in the fact whether or not the ischemia is serious enough to cause myocardial damage of such an extent that will cause the release of a sufficient amount of serum cardiac biomarkers so that these can be discovered and measured in serum (for example, cardiac troponin). The key role in ACS is played by atherosclerosis, atherosclerotic plaque and plaque rupture, in combination with thrombosis as an event of paramount importance--thrombosis.

[Invasive approach to patients with acute coronary syndrome]. / Invazivni pristup bolesniku s akutnim koronarnim sindromom--perkutane koronarne intervencije.

Cardiovascular diseases are the leading cause of mortality in Croatia. In concordance with this epidemiologic situation, a new organization of emergency medicine and a network of invasive cardiac laboratories have been introduced throughout Croatia. Main goal of this structuring is to improve the care of patients with acute coronary syndrome (ACS). The aim of this paper is to open discussion on the optimal way of treatment in patients with ACS in our country today, in the era of interventional cardiology of the 21st century. The pathophysiology of ACS encompasses a complex atheroinflammatory and atherothrombotic process with dynamic and progressive mechanical obstruction of coronary arteries and subsequently oxygen supply-demand mismatch. Conversely, the best way to treat such patients is reperfusion therapy, a goal nowadays achieved by either antithrombotic medical therapy or percutaneous coronary intervention (PCI). The weight of evidence does support the use of primary PCI as a standard and supreme reperfusion therapy, especially in myocardial infarction with ST elevation. The logistic complexities such as triage, transportation, the development of capable interventional center working 24-hours, even in developed countries, may be a major problem to use such a practice in the whole community. In ACS with non ST elevation, problems are even broader and include the importance of using optimal revascularization procedure (even cardiac surgery), timing and concomitant medical therapy, with certain stratification of every individual. Finally, especially for our country, medical and economic resources should be used optimally in order to achieve an optimal system to treat patients with ACS.

Donor heart selection and outcomes: An analysis of over 2,000 cases.

BACKGROUND: Decision-making when offered a donor heart for transplantation is complex, and supportive data describing outcomes according to acceptance or non-acceptance choices are sparse. Our aim was to analyze donor heart acceptance decisions and associated outcomes at a single center, and after subsequent acceptance elsewhere. METHODS: This investigation was a retrospective analysis of data obtained from the University of Vienna Medical Center and Eurotransplant centers for the period 2001 to 2015. RESULTS: Our center accepted 31.8% (699 of 2,199) of donor hearts offered. Unlike other centers, the acceptance rate, with or without transplantation, did not increase over time. Of the donor hearts rejected by our center, 38.1% (572 of 1,500) were later accepted elsewhere. Acceptance rates were twice as high for donor hearts initially rejected for non-quality reasons (339 of 601, 56.4%) compared with initial rejection for quality reasons (233 of 899, 25.9%). Three-year patient survival rate was 79% at Vienna; for donor hearts initially rejected by Vienna for non-quality reasons or quality reasons, it was 73% and 63%, respectively (p < 0.001). Outcomes at other centers after transplantation of grafts rejected by Vienna varied according to the reason for rejection, with good 3-year survival rates for rejection due to positive virology (77%), high catecholamines (68%), long ischemic time (71%), or low ejection fraction (68%), but poor survival was observed for hearts rejected for hypernatremia (46%), cardiac arrest (21%), or valve pathology (50%). CONCLUSIONS: A less restrictive policy for accepting donor hearts at our center, particularly regarding rejection for non-quality reasons or for positive virology, high catecholamine levels, longer ischemic time, or low ejection fraction, could expand our donor pool while maintaining good outcomes.

BPC 157 counteracts QTc prolongation induced by haloperidol, fluphenazine, clozapine, olanzapine, quetiapine, sulpiride, and metoclopramide in rats.

AIM: Commonly, neuroleptics and prokinetics induce a prolonged QTc interval. In this study, stable gastric pentadecapeptide BPC 157 counteracts the prolongation of the QTc interval in Wistar rats that underwent daily administration of dopamine neuroleptics or prokinetics. Previously, in rats and mice, BPC 157 counteracted neuroleptic-induced catalepsy and gastric ulcers. MAIN METHODS: To counteract neuroleptic- or prokinetic-induced prolongation of the QTc interval, rats were given a BPC 157 regimen once daily over seven days (10µg, 10ng/kg ip) immediately after each administrations of haloperidol (0.625, 6.25, 12.5, and 25.0mg/kg ip), fluphenazine (0.5, 5.0mg/kg ip), clozapine (1.0, 10.0mg/kg ip), quetiapine (1.0, 10.0mg/kg ip), sulpiride (1.6, 16.0mg/kg ip), metoclopramide (2.5, 25.0mg/kg ip) or (1.0, 10.0mg/kg ip). Controls simultaneously received saline (5ml/kg ip). To assess the ECG presentation before and after neuroleptic/prokinetic medication, the assessment was at 1, 2, 3, 4, 5, 10, 15, 20 and 30min (first administration) as well as at 30min, 60min and 24h (first administration and subsequent administrations) and the ECG recording started prior to drug administration. KEY FINDINGS: Since very early, a prolonged QTc interval has been continually noted with haloperidol, fluphenazine, clozapine, olanzapine, quetiapine, sulpiride, and metoclopramide in rats as a central common effect not seen with domperidone. Consistent counteraction appears with the stable gastric pentadecapeptide BPC 157. Thus, BPC 157 rapidly and permanently counteracts the QTc prolongation induced by neuroleptics and prokinetics. SIGNIFICANCE: Pentadecapeptide BPC 157 is suited for counteracting a prolonged QT interval.

Stable gastric pentadecapeptide BPC 157 and bupivacaine.

Bupivacaine toxicity following accidental overdose still lacks therapeutic solution. However, there are major arguments for testing BPC 157 against bupivacaine toxicity in vivo in rats, in particular, and then finally, in vitro. These are: the lack of any known BPC 157 toxicity, a lifesaving effect via the mitigation of arrhythmias in rats underwent hyperkalemia or digitalis toxicity, the elimination of hyperkalemia and arrhythmias in rats underwent succinylcholine toxicity and finally, the reduction of potassium-induced depolarization in vitro (in HEK293 cells) in severe hyperkalemia. Most importantly, BPC 157 successfully prevents and counteracts bupivacaine cardiotoxicity; BPC 157 is effective even against the worst outcomes such as a severely prolonged QRS complex. Here, rats injected with bupivacaine (100mg/kg IP) exhibited bradycardia, AV-block, ventricular ectopies, ventricular tachycardia, T-wave elevation and asystole. All of the fatalities had developed T-wave elevation, high-degree AV-block, respiratory arrest and asystole. These were largely counteracted by BPC 157 administration (50µg/kg, 10µg/kg, 10ng/kg, or 10pg/kg IP) given 30min before or 1min after the bupivacaine injection. When BPC 157 was given 6min after bupivacaine administration, and after the development of prolonged QRS intervals (20ms), the fatal outcome was markedly postponed. Additionally, the effect of bupivacaine on cell membrane depolarization was explored by measuring membrane voltages (Vm) in HEK293 cells. Bupivacaine (1mM) alone caused depolarization of the cells, while in combination with BPC 157 (1µm), the bupivacaine-induced depolarization was inhibited. Together, these findings suggest that the stable gastric pentadecapeptide BPC 157 should be a potential antidote for bupivacaine cardiotoxicity.

Role of echocardiography in diagnosis and management of complete papillary muscle rupture caused by myocardial infarction.

AIM: To evaluate the usefulness of echocardiography in the diagnosis of complete rupture of papillary muscle. METHODS: Transthoracic (TTE) and transesophageal echocardiography (TEE) was performed with the ATL 3000 HDI Ultrasound Inc (Bothell, WA, USA) with a 2.5 MHz transducer and 5-7 MHz multiplane phased array transducer. We are reporting about two patients (a 45 and a 51-year old male) with complete ruptures of papillary muscle following acute myocardial infarction (AMI). RESULTS: Both patients were previously treated with fibrinolysis in their local hospitals, 400 and 300 km, respectively, away from our hospital. Massive mitral regurgitation developed in both followed by rapid deterioration of hemodynamic state and severe heart failure, because of which both were transferred by helicopter to the Coronary Care Unit of our clinic. The diagnosis of complete papillary muscle rupture was confirmed in both patients by TTE and TEE. Due to the significant deterioration in their hemodynamic state, vasoactive drugs and intra-aortic balloon pump support were applied. Both patients then underwent mitral valve replacement, accompanied by concomitant coronary artery bypass grafting in one case. CONCLUSION: Transesophageal echocardiography is a more accurate and rapid diagnostic method in patients with mechanical complications of AMI than TTE.

Tetralogy of Fallot with cor triatriatum dexter in an adult patient: a case report.

Tetralogy of Fallot (TOF) is the most common cyanotic congenital heart defect with only approximately 3% of uncorrected patients surviving past age 40. In this case report, we present a 48-year-old mentally retarded man suffering from congenital spastic quadriplegia who was diagnosed with a unique combination of symptomatic TOF and cor triatriatum dexter (CTD). Reduced preload because of CTD with spastic quadriplegia that prevented physical exertion is believed to have facilitated this patient's unusually long survival.

Mortal hyperkalemia disturbances in rats are NO-system related. The life saving effect of pentadecapeptide BPC 157.

We demonstrate the full counteracting ability of stable gastric pentadecapeptide BPC 157 against KCl-overdose (intraperitoneal (i), intragastric (ii), in vitro (iii)), NO-system related. (i) We demonstrated potential (/kg) of: BPC 157 (10ng, 10µg ip, complete counteraction), l-arginine (100mg ip, attenuation) vs. L-NAME (5mg ip, deadly aggravation), given alone and/or combined, before or after intraperitoneal KCl-solution application (9mEq/kg). Therapy was confronted with promptly unrelenting hyperkalemia (>12mmol/L), arrhythmias (and muscular weakness, hypertension, low pressure in lower esophageal and pyloric sphincter) with an ultimate and a regularly inevitable lethal outcome within 30min. Previously, we established BPC 157-NO-system interaction; now, a huge life-saving potential. Given 30min before KCl, all BPC 157 regimens regained sinus rhythm, had less prolongation of QRS, and had no asystolic pause. BPC 157 therapy, given 10min after KCl-application, starts the rescue within 5-10min, completely restoring normal sinus rhythm at 1h. Likewise, other hyperkalemia-disturbances (muscular weakness, hypertension, low sphincteric pressure) were also counteracted. Accordingly with NO-system relation, deadly aggravation by L-NAME: l-arginine brings the values to the control levels while BPC 157 always completely nullified lesions, markedly below those of controls. Combined with l-arginine, BPC 157 exhibited no additive effect. (ii) Intragastric KCl-solution application (27mEq/kg) - (hyperkalemia 7mmol/L): severe stomach mucosal lesions, sphincter failure and peaked T waves were fully counteracted by intragastric BPC 157 (10ng, 10µg) application, given 30min before or 10min after KCl. (iii). In HEK293 cells, hyperkalemic conditions (18.6mM potassium concentrations), BPC 157 directly affects potassium conductance, counteracting the effect on membrane potential and depolarizations caused by hyperkalemic conditions.