2018 Vol. 15, No. 5
Not Applicable (Letter to the Editor)
Background Echocardiography has been shown to be a valuable resource in the diagnosis of many cardiac conditions, and can be used in all age groups, from the fetus to the oldest old. In the context of an increasingly aging population, the impact and utility of echocardiography in centenarians is largely unknown. This study is to determine whether echocardiography in centenarians aids in making clinical patient management decisions. Methods A retrospective review of echocardiograms from 1986 to 2014, at two affiliated tertiary centers, in individuals who were 100 years or older at the time of the examination. Patient and echocardiogram characteristics, management decisions based on echocardiography, and mortality were documented. Results 114 centenarians had echocardiograms, with ages ranging from 100 to 107 years (101 ± 1.4 years). In 82 of the centenarians evaluated (72%), no changes in management occurred as a consequence of the echocardiogram. From all management changes directly related to the echocardiogram, 81% (n = 26) of these corresponded to medication adjustments; interventional or surgical procedures followed the echocardiogram only in 4% (n = 5) of the total number of centenarians. Echocardiogram-based changes in management were only significant in patients that were referred for congestive heart failure (P = 0.02). After the echocardiogram was performed, 1-month and 1-year mortality were 15% and 47%, respectively. The median survival after the echocardiogram was obtained was 13 months (range 0.03 to 145 months), with no difference if there was a change or no change in management (P = 0.21). Conclusions Among centenarians undergoing echocardiography, despite additional diagnostic information, echocardiograms in centenarians influence management in a minority of cases, most commonly in the form of medication changes for treatment of heart failure. A significant proportion of centenarians are deceased within a year of undergoing echocardiographic assessment. These findings may question the overall utility of echocardiography in these late survivors.
Objective To investigate the role of sphingosine-1-phosphate (S1P) and its receptors in cardiomyocyte autophagy, cardiomyocyte hypertrophy and cardiac function. Methods Cardiomyocytes were isolated from neonatal Vista rats. Autophagy and hypertrophy of cardiomyocytes were induced via starvation culture and phenylephrine (PE), respectively, and S1P was used to treat the cardiomyocytes. The effect of S1P on cardiomyocyte autophagy was evaluated by the number of autophagosomes, the expression of autophagy-related proteins and autophagic marker genes in cardiomyocytes. The effect of S1P on cardiomyocyte hypertrophy was evaluated by examining the surface area of cardiomyocytes and the expression of hypertrophic genes. Subsequently, different small interfering RNAs (siRNAs) were used to knockdown the expression of the three types of S1P receptors on cardiomyocytes and to analyze the type of receptor that mediates S1P signaling in cardiomyocytes. Finally, sphingosine 1 phosphate receptor-1 (S1PR1) was knockout in the mouse cardiomyocytes using the Cas9 technique. The effect of S1PR1 on cardiac autophagy and cardiac hypertrophy was examined by assessing cardiomyocyte autophagy, cardiomyocyte hypertrophy and cardiac function. Results Starvation-induced cardiomyocyte autophagy and PE -induced cardiomyocyte hypertrophy were significantly attenuated by S1P. The results showed that the formation of autophagosomes was decreased, the autophagy-associated protein LC3Ⅱ/Ⅰ and the expression of autophagic marker genes Atg5, Atg12, Beclin1 and LC3B decreased after S1P treatment. The surface area of the cardiomyocytes was decreased, and the expression of hypertrophic genes, including atrial natriuretic factor (ANF), skeletal muscle and cardiac actin (SKA), myosin heavy chain (β-MHC) and brain natriuretic peptide (BNP) were all decreased after S1P treatment. The autophagy and hypertrophy of cardiomyocytes in the S1PR1 knocked-down group were significantly increased compared to those in the control group, the S1PR2 and the S1PR3 knocked-down groups. In vivo, the knockout of S1PR1 in cardiomyocytes exacerbated stress-induced cardiac autophagy, cardiac hypertrophy and the impairment of cardiac function. Conclusion S1P could inhibit cardiomyocyte autophagy, thereby inhibiting cardiomyocyte hypertrophy and protecting cardiac function by activating S1PR1 in pressure-overloaded cardiomyocytes in mice.
Objective The aim is to evaluate the association between baseline platelet count (PC) and severe adverse outcomes following percutaneous coronary intervention (PCI) in current real-world practice. Methods A total of 18,788 patients underwent PCI with drug-eluting stents constituted the study population. Patients were categorized as having low (Results In-hospital mortality rates for patients with low, normal, and high baseline PC were 0.6%, 0.4%, and 0.4%, respectively (P = 0.259). Similarly, mortality rates during long-term follow-up (median 23.8 months) for patients with low, normal, and high baseline PC were 0.9%, 0.6%, and 0.7%, respectively (P = 0.079). After multivariate adjustment, patients with low or high baseline PC tended to have similar risks for both in-hospital and follow-up mortality compared with the normal group. Subgroup analyses failed to demonstrate an independent prognostic value of baseline PC in specific population groups except patients who undwent transfemoral PCI. There was also no significant difference in the incidence of major bleeding requiring a blood transfusion in the low, normal, and high groups (0.5%, 0.3%, and 0.3%, respectively; P = 0.320). After multivariate adjustment, low or high baseline PC did not signi?ficantly increase the risk of major bleeding. Conclusion There is no significant association between baseline PC and severe adverse outcomes following PCI in current real-world practice.
Background Studies have shown that staged percutaneous coronary intervention (PCI) for non-culprit lesions is beneficial for prognosis of ST-segment elevation myocardial infarction (STEMI) patients with multivessel disease. However, the optimal timing of staged revascularization is still controversial. This study aimed to find the optimal timing of staged revascularization. Methods A total of 428 STEMI patients with multivessel disease who underwent primary PCI and staged PCI were included. According to the time interval between primary and staged PCI, patients were divided into three groups (≤ 1 week, 1–2 weeks, and 2–12 weeks after primary PCI). The primary endpoint was major adverse cardiovascular events (MACE), a composite of all-cause death, non-fatal re-infarction, repeat revascularization, and stroke. Cox regression model was used to assess the association between staged PCI timing and risk of MACE. Results During the follow-up, 119 participants had MACEs. There was statistical difference in MACE incidence among the three groups (≤ 1 week: 23.0%; 1–2 weeks: 33.0%; 2–12 weeks: 40.0%; P = 0.001). In the multivariable adjustment model, the timing interval of staged PCI ≤ 1 week and 1–2 weeks were both significantly associated with a lower risk of MACE [hazard ratio (HR): 0.40, 95% confidence intervals (CI): 0.24–0.65; HR: 0.54, 95% CI: 0.31–0.93, respectively], mainly attributed to a lower risk of repeat revascularization (HR: 0.41, 95% CI: 0.24–0.70; HR: 0.36, 95% CI: 0.18–0.7), compared with a strategy of 2–12 weeks later of primary PCI. Conclusions The optimal timing of staged PCI for non-culprit vessels should be within two weeks after primary PCI for STEMI patients.
Background The objective of this study was to identify prognostic indicators in patients with inflammatory cardiomyopathy (iCM) on endomyocardial biopsy (EMB). Methods and results Between 2007 and 2011 all consecutive patients with diagnosed with iCM at EMB were retrospectively analyzed. The combined primary endpoint (EP) (1°EP) was cardiac death, aborted sudden cardiac death/appropriate implantable cardioverter defibrillator (ICD) shock, progressive heart failure requiring left ventricular assist device (LVAD) implantation and heart transplantation. 503 patients (mean age 58 ± 12 years, 73% male) were available for analysis. Genomes of cardiotrophic viruses were detected in 396 patients (79%) and immuno-histochemical signs of inflammation were present in 223 individuals (44%). After 3.6 ± 2.4 years of follow-up, cardiac mortality was 3.0% (n = 14) and a total of 8.6% (n = 40) reached the primary endpoint. Independent predictors for the 1°EP were: age ≥ 50 years, presence and duration (≤ 28 days) of symptomatic heart failure. A risk stratification approach based on the results of the multivariate analysis demonstrated that absence of signs and/or symptoms of congestive heart failure in younger ( 28 days) duration of disease appear to have an excellent prognosis with 100% survival and no events during follow-up. The presence of all above mentioned independent risk factors results in an 1°EP occurrence of 35.9%. Conclusions Symptoms of heart failure, short duration of disease, and older age are indicators of poor outcome in patients with iCM.
Persistent ductus arteriosus is a congenital cardiovascular malformation usually diagnosed in early childhood by echocardiography and cardiac catheterization. Computed tomography and cardiac magnetic resonance are excellent, noninvasive methods and are recommended when additional quantification of RV, LV, shunt a or PAH is required. We present a case of an 86-year-old woman with symptoms of a continuous murmur, heart failure (shortness of breath and fatigue) and atrial fibrillation. The 24-hour-monitoring of the electrocardiogram showed the average heart rhythm 69bpm and with 80 pauses above 2.0 seconds which were asymptomatic. Echocardiography showed features of pulmonary hypertension. Computed tomography excluded pulmonary embolism but suggested the suspicion of persistent ductus arteriosus. To find the cause of pulmonary hypertension, a magnetic resonance was performed which showed persistent ductus arteriosus. A treatment with ACE inhibitors, rivaroxaban, etc. was applied. Due to the clinical status of the patient and the lack of consent for PDA closure, a conservative treatment was proposed. Congenital heart disease in elderly patients is challenging. Cardiac magnetic resonance imaging is non-invasive and quantifies accurately the cause of pulmonary hypertension in elderly patients with an undiagnosed congenital heart disease. Furthermore, it can be safely performed to monitor pulmonary hypertension without the risk of ionizing radiation.
Elderly patients, especially women often present atypical symptoms and chest pain may be wrong diagnosed. We present a patient who was admitted to the hospital two times because of the similar symptoms but diagnosis was completely different. Most researchers believe that significant changes in the coronary arteries exclude the diagnosis of takotsubo syndrome (TTS). However, some reports admit the possibility of coexistence of TTS and coronary artery disease. Presented patient had not had any changes in coronary arteries until four years later when she had myocardial infarction associated with right coronary artery narrowing, despite the fact that the risk factors of coronary heart disease were closely monitored. It is very important to maintain a high index of suspicion for acute myocardial infarction in elderly patients even if symptoms and past medical history suggest alternative diagnosis.
A 70-year-old female visited our hospital due to long-standing persistent atrial fibrillation and underwent hybrid atrial fibrillation procedure. This is the first case of sequential hybrid procedure using automated ultra-high density mapping system. The ultra-high density mapping would enable a better understanding of different arrhythmogenic substrate and facility sequential hybrid atrial fibrillation procedure.
Ventricular noncompaction (VNC) is an unusual cause of cardiomyopathy. The most common site of involvement is the left ventricle, with isolated right ventricular noncompaction (iRVNC) involvement being reported in a few cases. No iRVNC caused pulmonary embolism (PE) has been reported so far. In this report, we present one case of iRVNC caused PE. The patient was admitted in my hospital due to aggravated chest tightness after activities, accompanied by breathlessness, repeated amaurosis, and syncope. Coronary and left ventricular angiography revealed no abnormality. Pulmonary angiography suggested bilateral PE and pulmonary arterial hypertension, and noncompaction of right ventricular myocardium was ocationally found in main pulmonary artery angiography, which was confirmed by right ventricular angiography and echocardiography and was diagnosed as iRVNC. Since no thrombus was found in venography in both lower limb varices, it was thought that the PE was caused by situ embolus of the right ventricle. This patient was applied thrombolysis, anticoagulation, and ventricular remodeling improvement, and appeared improved conditions. The very rare case warns us when PE occurs while without significant risk factors or lower extremity deep venous thrombosis (DVT), iRVNC should be considered.