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Marijuana is the most widely used illicit drug, with approximately 200 million users worldwide. Once illegal throughout the United States, cannabis is now legal for medicinal purposes in several states and for recreational use in 3 states. The current wave of decriminalization may lead to more widespread use, and it is important that cardiologists be made aware of the potential for marijuana-associated adverse cardiovascular effects that may begin to occur in the population at a greater frequency. In this report, the investigators focus on the known cardiovascular, cerebrovascular, and peripheral effects of marijuana inhalation. Temporal associations between marijuana use and serious adverse events, including myocardial infarction, sudden cardiac death, cardiomyopathy, stroke, transient ischemic attack, and cannabis arteritis have been described. In conclusion, the potential for increased use of marijuana in the changing legal landscape suggests the need for the community to intensify research regarding the safety of marijuana use and for cardiologists to maintain an awareness of the potential for adverse effects.

There is evidence that certain stressors can trigger cardiovascular events. Several studies have now demonstrated an increase in major adverse cardiac events associated with natural disasters such as an earthquake. The purpose of this paper is to review the literature on earthquakes and cardiovascular events. Reports from 13 major quakes were reported. Earthquakes have been associated with a number of cardiac events including sudden cardiac death, fatal myocardial infarction (MI), myocardial infarction, stress cardiomyopathy, heart failure, stroke, arrhythmias, hypertension and pulmonary embolism. Most reports were associated with earthquakes of magnitude 6.0 or greater. Cardiac events were reported within hours of the quakes. In some reports there was a sharp spike in cardiac events followed by a decrease; but in other quakes the increases in cardiac events lasted weeks, months and even years. There often was an association between the cardiac events and amount of personal property loss. The Great East Japan Earthquake was an unusual event in that it was associated with a major tsunami and cardiac events appeared worse in inundated areas due to flooding. Some but not all reports suggested more MIs associated with early morning earthquakes that woke up the population. Hospitals in earthquake-prone areas should consider developing plans for handling increases in myocardial infarctions and other cardiac events that are associated with earthquakes.

The heart and brain have bi-directional influences on each other, including autonomic regulation and hemodynamic connections. Heart rate variability (HRV) measures variation in beat-to-beat intervals. New findings about disorganized sinus rhythm (erratic rhythm, quantified as heart rate fragmentation, HRF) are discussed and suggest overestimation of autonomic activities in HRV changes, especially during aging or cardiovascular events. When excluding HRF, HRV is regulated via the central autonomic network (CAN). HRV acts as a proxy of autonomic activity and is associated with executive functions, decision-making, and emotional regulation in our health and wellbeing. Abnormal changes of HRV (e.g., decreased vagal functioning) are observed in various neurological conditions including mild cognitive impairments, dementia, mild traumatic brain injury, migraine, COVID-19, stroke, epilepsy, and psychological conditions (e.g., anxiety, stress, and schizophrenia). Efforts are needed to improve the dynamic and intriguing heart-brain interactions.

The adult mammalian heart has limited capability for self-repair after myocardial infarction. Therefore, therapeutic strategies that improve post-infarct cardiac function are critically needed. The small molecule ICG-001 modulates Wnt signaling and increased the expression of genes beneficial for cardiac regeneration in epicardial cells. Lineage tracing experiments, demonstrated the importance of β-catenin/p300 mediated transcription for epicardial progenitor contribution to the myocardium. Female rats given ICG-001 for 10 days post-occlusion significantly improved ejection fraction by 8.4%, compared to controls (P<0.05). Taken together, Wnt modulation via β-catenin/CBP inhibition offers a promising therapeutic strategy towards restoration of myocardial tissues and an enhancement of cardiac functions following infarction.

Sodium-glucose co-transporter 2 (SGLT2) inhibitors have demonstrated potential neuroprotective and cardioprotective effects in preliminary studies. This study evaluates the efficacy of empagliflozin (EMPA) in reducing ischemia/reperfusion damage in both the brain and heart using rat models. Ischemic stroke and myocardial infarction (MI) were induced in male Sprague-Dawley rats, which were randomized into three groups: (1) Control (no EMPA), (2) Acute treatment (EMPA, 10 mg/kg IV, administered 10 min before ischemia and 1 min before reperfusion), and (3) Chronic treatment (EMPA, 20 mg/kg in food for 7 days before ischemia). Stroke was induced by middle cerebral artery occlusion (MCAO) for one hour, followed by 3 h of reperfusion, and MI was induced by left coronary artery occlusion for 30 min, followed by 3 h of reperfusion. Brain and heart tissues were analyzed for anatomic size of myocardial infarction and stroke. In the brain, cerebral infarction was significantly smaller in both EMPA treatment groups compared to controls (acute: 3.7 ± 1.2%, chronic: 6.9 ± 2.1% vs. control: 14.5 ± 2.5%, p < 0.05). Edema was also reduced in the EMPA groups (acute: 5.5 ± 0.9%, chronic: 5.9 ± 0.8% vs. control: 9.6 ± 1.2%, p < 0.05). In the heart, MI size was significantly reduced in both EMPA groups (acute: 46.9 ± 2.0%, chronic: 48.8 ± 5.8% vs. control: 70.0 ± 2.6%, p < 0.05), and no-reflow size was smaller in the EMPA groups (acute: 36.3 ± 3.3%, chronic: 33.9 ± 4.3% vs. control: 53.4 ± 3.3%, p < 0.05). EMPA treatment, both acute and chronic, significantly reduces cerebral infarct volume and edema, as well as myocardial infarct size and no-reflow in rat models of ischemic stroke and myocardial ischemia/reperfusion, indicating substantial neuroprotective and cardioprotective effects.

As more patients survive myocardial infarctions, the incidence of heart failure increases. After an infarction, the human heart undergoes a series of structural changes, which are governed by cellular and molecular mechanisms in a pathological metamorphosis termed “remodeling.” This review will discuss the current developments in our understanding of these molecular and cellular events in remodeling and the various pharmacological, cellular and device therapies used to treat, and potentially retard, this condition. Specifically, this paper will examine the neurohormonal activity of the renin–angiotensin–aldosterone axis and its molecular effects on the heart. The emerging understanding of the extra-cellular matrix and the various active molecules within it, such as the matrix metalloproteinases, elicits new appreciation for their role in cardiac remodeling and as possible future therapeutic targets. Cell therapy with stem cells is another recent therapy with great potential in improving post-infarcted hearts. Lastly, the cellular and molecular effects of left ventricular assist devices on remodeling will be reviewed. Our increasing knowledge of the cellular and molecular mechanisms underlying cardiac remodeling enables us not only to better understand how our more successful therapies, like angiotensin-converting enzyme inhibitors, work, but also to explore new therapies of the future.

Background While the acute exposure to electronic cigarette (E-cig) vapor has been associated with an increase in blood pressure, the chronic effect of E-cig vapor on blood pressure compared to standard cigarette smoke has not been extensively studied. We determined the effect of E-cig exposure on blood pressure and other measures of cardiac function in both young and old rats. Methods Young Sprague Dawley rats (6 weeks old, both sexes) were randomly exposed to air ( n  = 34), E-cig with nicotine (E-cig Nic+; n  = 30), E-cig without nicotine (E-cig Nic-; n  = 28) or standard cigarette smoke ( n  = 27). Old Fischer 344 rats (25 months old, both sexes) were randomized into 2 groups: (1) 26 rats in the purified air (negative control) group and (2) 17 rats in the electronic cigarette vapor plus nicotine group (E-cig Nic+). After 12 weeks of exposure, hemodynamics were determined by Millar catheter, echocardiography, and thermodilution catheter, a few days after their last exposure. Results In young rats, cigarette smoke was associated with higher systolic, diastolic and mean blood pressures and peak LV systolic pressure, compared to air or E-cig Nic + or E-cig Nic- groups. Neither fractional shortening nor cardiac output differed among the groups. Absolute value for dp/dt min, a measure of diastolic LV function, was lowest in the E-cig Nic- group. Tau, a measure of LV relaxation was worse in this group as well. In old rats, E-cig vaping did not change heart rate, blood pressure, and cardiac function. However, E-cig Nic + exposure was associated with a greater heart weight/BW and LV weight/BW compared to air exposure in old rats. Conclusions Chronic exposure to E-cig vaping did not cause an increase in blood pressure or heart rate, nor did it change cardiac function compared to air in young rats after 12 weeks of exposure, while standard cigarette smoking was associated with an increase in blood pressure. E-cig vaping was associated with a greater heart weight/BW and LV weight/BW compared to air exposure in old rats, suggested that older animals might be more vulnerable to E-cig stimulus than younger ones.

Key Points Mortality after acute ST-segment elevation myocardial infarction (STEMI) has plateaued in the past decade, after a period of continual decline Beyond early reperfusion, a variety of adjunctive agents to reduce myocardial infarction after reperfusion have been tested in clinical settings, and have yielded largely disappointing results Before clinical testing, candidate cardioprotective agents should be tested in animal models with comorbidities similar to that in patients, and in combination with P2Y 12 inhibitors Approaches for improving cardiac function following STEMI that have been promising in preclinical studies include those that target mitochondrial bioenergetics, pyroptosis, autophagy, and no-reflow and anaesthetic preconditioning Strategies to reduce myocardial infarct size beyond early reperfusion have thus far yielded disappointing results in clinical trials. In this Review, Kloner and co-workers discuss several new approaches to preserve the reperfused myocardium, including those that target mitochondrial bioenergetics and autophagy. Early coronary artery reperfusion improves outcomes for patients with ST-segment elevation myocardial infarction (STEMI), but morbidity and mortality after STEMI remain unacceptably high. The primary deficits seen in these patients include inadequate pump function, owing to rapid infarction of muscle in the first few hours of treatment, and adverse remodelling of the heart in the months that follow. Given that attempts to further reduce myocardial infarct size beyond early reperfusion in clinical trials have so far been disappointing, effective therapies are still needed to protect the reperfused myocardium. In this Review, we discuss several approaches to preserving the reperfused heart, such as therapies that target the mechanisms involved in mitochondrial bioenergetics, pyroptosis, and autophagy, as well as treatments that harness the cardioprotective properties of inhaled anaesthetic agents. We also discuss potential therapies focused on correcting the no-reflow phenomenon and its effect on healing and adverse left ventricular remodelling.

Sodium serves as one of the primary cations in the central nervous system, playing a crucial role in maintaining normal brain function. In this study, we investigated alterations in sodium concentrations in the brain and/or cerebrospinal fluid across multiple models, including an aging model, a stroke model, a nitroglycerin (NTG)-induced rat migraine model, a familial hemiplegic migraine type 2 (FHM2) mouse model, and a transgenic mouse model of Alzheimer’s disease (AD). Our results reveal that older rats exhibited higher sodium concentrations in cerebrospinal fluid (CSF), plasma, and various brain regions compared to their younger counterparts. Additionally, findings from the stroke model demonstrated a significant increase in sodium in the ischemic/reperfused region, accompanied by a decrease in potassium and an elevated sodium/potassium ratio. However, we did not detect significant changes in sodium in the NTG-induced rat migraine model or the FHM2 mouse model. Furthermore, AD transgenic mice showed no significant differences in sodium levels compared to wild-type mice in CSF, plasma, or the hippocampus. These results underscore the nuanced regulation of sodium homeostasis in various neurological conditions and aging, providing valuable insights into potential mechanisms underlying these alterations.

Alterations in functional connectivity (FC) have been observed in individuals with Alzheimer’s disease (AD) with elevated amyloid ( A β ) and tau. However, it is not yet known whether directed FC is already influenced by A β and tau load in cognitively healthy (CH) individuals. A 21-channel electroencephalogram (EEG) was used from 46 CHs classified based on cerebrospinal fluid (CSF) A β tau ratio: pathological (CH-PAT) or normal (CH-NAT). Directed FC was estimated with Partial Directed Coherence in frontal, temporal, parietal, central, and occipital regions. We also examined the correlations between directed FC and various functional metrics, including neuropsychology, cognitive reserve, MRI volumetrics, and heart rate variability between both groups. Compared to CH-NATs, the CH-PATs showed decreased FC from the temporal regions, indicating a loss of relative functional importance of the temporal regions. In addition, frontal regions showed enhanced FC in the CH-PATs compared to CH-NATs, suggesting neural compensation for the damage caused by the pathology. Moreover, CH-PATs showed greater FC in the frontal and occipital regions than CH-NATs. Our findings provide a useful and non-invasive method for EEG-based analysis to identify alterations in brain connectivity in CHs with a pathological versus normal CSF A β /tau. This study reveals disrupted brain functional connectivity as an early biomarker in cognitively healthy individuals with pathological CSF amyloid/tau, aiding early Alzheimer’s detection.